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Ojukwu CP, Nnyaba IS, Ede SS, Okemuo AJ, Enebe JA. The effect of rebound exercise on cognition and balance of females with overweight and obesity. Libyan J Med 2025; 20:2438513. [PMID: 39643930 PMCID: PMC11626867 DOI: 10.1080/19932820.2024.2438513] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/22/2024] [Accepted: 12/03/2024] [Indexed: 12/09/2024] Open
Abstract
Balance issues have been reported to be common among females with overweight or obesity with associated fall risks. Despite the increasing reports of the negative impacts of obesity on balance and cognition, there is a scarcity of research aimed at evaluating effective interventions. To examine the effects of rebound exercises on cognition and balance among females with overweight and obesity. This Quasi-experimental study used the purposive sampling method to recruit 20 female students (aged 17-35 years) with overweight and obese at the Evangel University Akaeze, Ebonyi State Nigeria. Rebound exercise intervention was administered to all participants at the gym for 30 minutes in each session, three times a week for six weeks, while their cognitive performances, stationary balance, and dynamic balance were measured pre-and post-trial using Trail Marking Test Apparatuses, Unilateral Pedal Tests, and Meter Backward Walk Test respectively. There was a significant (p < 0.001) difference in the participants' cognition values across weeks 1, 3, and 6 with a progressive improvement over time. There was also a significant (p < 0.05) difference in the participants' static and dynamic balance values across weeks 1, 3, and 6 with a progressive improvement in balance performance over time. Rebound exercise significantly improved the cognition and balance of females with overweight or obese. This finding suggests a promising intervention to improve balance and cognitive-related problems in this population. Registered retrospectively in the Pan African Clinical Trial Registry, identification number for the registry is PACTR202405746557031. Dated 2 May 2024.
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Affiliation(s)
| | - Izuchukwu Simeon Nnyaba
- Department of Physiotherapy, College of Health Sciences, Evangel University, Akaeze, Ebonyi, Nigeria
| | - Stephen Sunday Ede
- School of Health, Social Work, and Sports, University of Central Lancashire, Preston, UK
| | - Adaora Justina Okemuo
- Department of Medical Rehabilitation, College of Medicine, University of Nigeria, Enugu, Nigeria
- School of Health and Social Care Professions, Buckinghamshire New University, High Wycombe, UK
| | - Judith Amaka Enebe
- Department of Physiotherapy, Faculty of Health Sciences and Technology, David Umahi Federal University of Health sciences, Uburu, Nigeria
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2
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Wang X, Liu C, Huang T, Xiao X, Zeng D, He L, Gong Z, Jiang B, Zhang X, Liu M. 1H NMR Reveals Predictive Metabolic Signatures of Response to RMP1-14 Treatment in the Plasma of Tumor-Bearing Mice. J Proteome Res 2025. [PMID: 40515704 DOI: 10.1021/acs.jproteome.5c00134] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 06/16/2025]
Abstract
Understanding and predicting individual responses to immune checkpoint inhibitors (ICIs) are of great importance for advancing precise cancer immunotherapy. This study utilizes 1H NMR-based plasma phenotyping to reveal the metabolic characteristics and predictive signatures of tumor-bearing mice that are sensitive and nonsensitive to the PD-1 inhibitor RMP1-14. Metabolite set enrichment analysis showed that the high-sensitivity (HS) group may exhibit a more robust immune profile by upregulating sphingolipid metabolism and lactose metabolism before treatment, while the enrichment of branched-chain amino acids and disorder of glucose and lipid metabolism in the low-sensitivity (LS) group may facilitate tumor growth and immune escape. 1H NMR information on glycoproteins and lipoproteins in predose plasma was significantly correlated with differences in treatment effects. This correlation was validated by the random forest prediction model constructed from the NMR information, which demonstrated a lower out-of-bag error rate. The model further suggested that acetyl-signaling GlycA and GlycB from N-acetyl glycoproteins of predose plasma are predictive signatures for the HS group, whereas lipid-related signals were predictive for the LS group. This study presents an NMR-based framework for investigating and predicting individual variability in responses to ICIs, providing a methodological and data-driven foundation for enhancing precision cancer immunotherapy.
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Affiliation(s)
- Xiaohua Wang
- State Key Laboratory of Magnetic Resonance Spectroscopy and Imaging, National Center for Magnetic Resonance in Wuhan, Wuhan Institute of Physics and Mathematics, Innovation Academy for Precision Measurement Science and Technology, Chinese Academy of Sciences, Wuhan, 430071, China
- University of Chinese Academy of Sciences, Beijing, 100049, China
| | - Caixiang Liu
- State Key Laboratory of Magnetic Resonance Spectroscopy and Imaging, National Center for Magnetic Resonance in Wuhan, Wuhan Institute of Physics and Mathematics, Innovation Academy for Precision Measurement Science and Technology, Chinese Academy of Sciences, Wuhan, 430071, China
- University of Chinese Academy of Sciences, Beijing, 100049, China
| | - Tao Huang
- State Key Laboratory of Magnetic Resonance Spectroscopy and Imaging, National Center for Magnetic Resonance in Wuhan, Wuhan Institute of Physics and Mathematics, Innovation Academy for Precision Measurement Science and Technology, Chinese Academy of Sciences, Wuhan, 430071, China
- University of Chinese Academy of Sciences, Beijing, 100049, China
| | - Xiongjie Xiao
- State Key Laboratory of Magnetic Resonance Spectroscopy and Imaging, National Center for Magnetic Resonance in Wuhan, Wuhan Institute of Physics and Mathematics, Innovation Academy for Precision Measurement Science and Technology, Chinese Academy of Sciences, Wuhan, 430071, China
- University of Chinese Academy of Sciences, Beijing, 100049, China
| | - Danyun Zeng
- State Key Laboratory of Magnetic Resonance Spectroscopy and Imaging, National Center for Magnetic Resonance in Wuhan, Wuhan Institute of Physics and Mathematics, Innovation Academy for Precision Measurement Science and Technology, Chinese Academy of Sciences, Wuhan, 430071, China
- University of Chinese Academy of Sciences, Beijing, 100049, China
| | - Lichun He
- State Key Laboratory of Magnetic Resonance Spectroscopy and Imaging, National Center for Magnetic Resonance in Wuhan, Wuhan Institute of Physics and Mathematics, Innovation Academy for Precision Measurement Science and Technology, Chinese Academy of Sciences, Wuhan, 430071, China
- University of Chinese Academy of Sciences, Beijing, 100049, China
| | - Zhou Gong
- State Key Laboratory of Magnetic Resonance Spectroscopy and Imaging, National Center for Magnetic Resonance in Wuhan, Wuhan Institute of Physics and Mathematics, Innovation Academy for Precision Measurement Science and Technology, Chinese Academy of Sciences, Wuhan, 430071, China
- University of Chinese Academy of Sciences, Beijing, 100049, China
| | - Bin Jiang
- State Key Laboratory of Magnetic Resonance Spectroscopy and Imaging, National Center for Magnetic Resonance in Wuhan, Wuhan Institute of Physics and Mathematics, Innovation Academy for Precision Measurement Science and Technology, Chinese Academy of Sciences, Wuhan, 430071, China
- University of Chinese Academy of Sciences, Beijing, 100049, China
- Wuhan National Laboratory for Optoelectronics, Huazhong University of Science and Technology, Wuhan, 430074, China
- Optics Valley Laboratory, Wuhan, 430074, China
| | - Xu Zhang
- State Key Laboratory of Magnetic Resonance Spectroscopy and Imaging, National Center for Magnetic Resonance in Wuhan, Wuhan Institute of Physics and Mathematics, Innovation Academy for Precision Measurement Science and Technology, Chinese Academy of Sciences, Wuhan, 430071, China
- University of Chinese Academy of Sciences, Beijing, 100049, China
- Wuhan National Laboratory for Optoelectronics, Huazhong University of Science and Technology, Wuhan, 430074, China
- Optics Valley Laboratory, Wuhan, 430074, China
| | - Maili Liu
- State Key Laboratory of Magnetic Resonance Spectroscopy and Imaging, National Center for Magnetic Resonance in Wuhan, Wuhan Institute of Physics and Mathematics, Innovation Academy for Precision Measurement Science and Technology, Chinese Academy of Sciences, Wuhan, 430071, China
- University of Chinese Academy of Sciences, Beijing, 100049, China
- Wuhan National Laboratory for Optoelectronics, Huazhong University of Science and Technology, Wuhan, 430074, China
- Optics Valley Laboratory, Wuhan, 430074, China
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Schoepf IC, Haerry D, Esteban-Cantos A, Arribas JR, Tarr PE. Perspective: clinical relevance of epigenetic aging and HIV. Epigenomics 2025:1-5. [PMID: 40231671 DOI: 10.1080/17501911.2025.2491299] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/30/2024] [Accepted: 04/07/2025] [Indexed: 04/16/2025] Open
Abstract
Longitudinal studies now document how leukocyte telomere attrition and epigenetic aging may be accelerated in people with HIV (PWH), in particular, around the time of HIV acquisition, during primary HIV infection, and during untreated chronic HIV infection. Whether chronic low-level inflammation and epigenetic aging go hand in hand or may be partially independent continues to be investigated in PWH and other settings. Epigenetic age acceleration (EAA) in PWH has now clearly been shown to be potentially reversible during successful antiretroviral therapy (ART). These studies point to how the beneficial effects of modern ART also include EAA-decelerating effects that seem large enough to regard ART as a kind of epigenetic rejuvenation therapy. Progress in the field has been limited in part due to the high cost of assessing EAA based on DNA methylation measures ("epigenetic clocks"). Demonstration of the clinical relevance of EAA and its reversion by ART will depend on large studies associating EAA with cardiovascular events and other adverse aging-associated endpoints in PWH.
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Affiliation(s)
- Isabella C Schoepf
- University Department of Medicine and Infectious Diseases Service, Kantonsspital Baselland, University of Basel, Bruderholz, Switzerland
- Department of Visceral Surgery and Medicine, Inselspital, Bern University Hospital, University of Bern, Bern, Switzerland
| | | | - Andrés Esteban-Cantos
- HIV/AIDS and Infectious Diseases Research Group, Hospital La Paz Institute for Health Research, Madrid, Spain
- CIBER of Infectious Diseases (CIBERINFEC), Madrid, Spain
| | - José R Arribas
- HIV/AIDS and Infectious Diseases Research Group, Hospital La Paz Institute for Health Research, Madrid, Spain
- CIBER of Infectious Diseases (CIBERINFEC), Madrid, Spain
| | - Philip E Tarr
- University Department of Medicine and Infectious Diseases Service, Kantonsspital Baselland, University of Basel, Bruderholz, Switzerland
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Schepanski S, Ngoumou GB, Koch AK, Schröter M, Roehle R, Seifert G. Mind-body therapies and their interplay with the immune system in children and adolescents: a protocol for a systematic review and meta-analysis. Syst Rev 2025; 14:78. [PMID: 40186267 PMCID: PMC11969903 DOI: 10.1186/s13643-025-02812-4] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/11/2024] [Accepted: 03/11/2025] [Indexed: 04/07/2025] Open
Abstract
BACKGROUND Chronic inflammation is a critical public health concern that, in children and adolescents, increases the long-term risk of a variety of different health issues. While mind-body therapies like yoga, meditation, and acupuncture have shown promise in modulating immune responses in adults, their safety and effectiveness in pediatric populations remain underexplored. This protocol outlines the methodology for a systematic review and meta-analysis aimed at evaluating the effects of mind-body therapies on immune modulation in children and adolescents. METHODS This systematic review and meta-analysis will follow PRISMA 2020 guidelines. We will include randomized controlled trials, non-randomized controlled trials, cohort studies, and case-control studies that examine the relationship between mind-body therapies and immune markers in pediatric populations. Electronic searches will be conducted in MEDLINE, Embase, PsycINFO, CINAHL, Web of Science, and the Cochrane Library, supplemented by trial registries. Risk of bias will be assessed using the Cochrane Risk of Bias Tool (RoB 1), the Risk of Bias in Non-randomized Studies of Interventions (ROBINS-I), and the Newcastle-Ottawa Scale (NOS). Two independent reviewers will screen studies, extract data, and assess study quality, with a third reviewer resolving any discrepancies. Results will be synthesized both narratively and through meta-analysis using R software. DISCUSSION The review will evaluate the effectiveness and safety of mind-body therapies on immune markers in children and adolescents. The synthesized evidence will guide clinical practice and public health policies in integrating mind-body therapies into pediatric care. The findings will also provide a foundation for future research and policymaking in this area. SYSTEMATIC REVIEW REGISTRATION PROSPERO CRD42024546585.
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Affiliation(s)
- Steven Schepanski
- Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Charité Competence Center for Traditional and Integrative Medicine (CCCTIM), Berlin, Germany.
- Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Pediatrics, Division of Oncology and Hematology, Berlin, Germany.
| | - Gonza B Ngoumou
- Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Charité Competence Center for Traditional and Integrative Medicine (CCCTIM), Berlin, Germany
- Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Pediatrics, Division of Oncology and Hematology, Berlin, Germany
| | - Anna Katharina Koch
- Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Charité Competence Center for Traditional and Integrative Medicine (CCCTIM), Berlin, Germany
- Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Pediatrics, Division of Oncology and Hematology, Berlin, Germany
| | - Marleen Schröter
- Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Charité Competence Center for Traditional and Integrative Medicine (CCCTIM), Berlin, Germany
- Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Pediatrics, Division of Oncology and Hematology, Berlin, Germany
| | - Robert Roehle
- Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Institute for Biometry and Clinical Epidemiology, Berlin, Germany
- Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Clinical Trial Office, Berlin, Germany
- Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Berlin Institute of Health, Berlin, Germany
| | - Georg Seifert
- Charité - Universitätsmedizin Berlin, Corporate Member of Freie Universität Berlin, Humboldt-Universität zu Berlin, Charité Competence Center for Traditional and Integrative Medicine (CCCTIM), Berlin, Germany
- Charité - Universitätsmedizin Berlin, corporate member of Freie Universität Berlin and Humboldt-Universität zu Berlin, Department of Pediatrics, Division of Oncology and Hematology, Berlin, Germany
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5
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Soremekun C, Jjingo D, Kateete D, Nash O, Nitsch D, Nyirenda M, Gill D, Zeggini E, Grallert H, Peters A, Chikowore T, Batini C, Soremekun O, Fatumo S. Mendelian randomization study highlights the role of hematological traits on Type-2 diabetes mellitus in African ancestry individuals. Front Pharmacol 2025; 16:1436972. [PMID: 40230699 PMCID: PMC11994964 DOI: 10.3389/fphar.2025.1436972] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/22/2024] [Accepted: 03/03/2025] [Indexed: 04/16/2025] Open
Abstract
Introduction Observational studies have identified associations between hematological traits and type-2 diabetes mellitus (T2D). However, it is difficult to infer causal effects due to the potential of confounding. Our study utilizes the Mendelian randomization (MR) approach to address the above limitation and investigate the causal effect of hematological traits such as white blood cell (WBC), platelets (PLT), and red blood cell (RBC) on T2D in individuals of African ancestry. Methods The participating cohorts included participants of African ancestry in the Blood Cell consortium and the Million Veteran Program dataset. Using GWAS summary statistics, we applied a univariable and multivariable Two-sample MR to estimate the causal relationship between hematological traits and T2D. Results In the main IVW MR estimates, genetically predicted levels of mean corpuscular hemoglobin concentration (MCHC), mean corpuscular hemoglobin (MCH), and mean corpuscular volume (MCV) were associated with decreased risk of T2D. We also observed a decreased risk of T2D with genetically predicted total WBC count and neutrophil count (NEU), for the WBC traits. The multivariable analysis further supported the direct associations of genetically predicted MCH, MCHC, and MCV levels with a decreased risk of T2D. For the European ancestry, a similar pattern of association was observed for MCH and MCV. Discussion These findings indicate that hematological traits may differentially play a role in the development of T2D and be affected by T2D. However, further research is needed to validate and explore the biological pathways and mechanisms involved in these associations.
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Affiliation(s)
- Chisom Soremekun
- The African Computational Genomics (TACG) Research Group, MRC/UVRI and LSHTM Uganda Research Unit, Entebbe, Uganda
- Department of Immunology and Molecular Biology, School of Biomedical Sciences, Makerere University College of Health Sciences, Kampala, Uganda
- Centre for Genomics Research and Innovation, NABDA/FMST, Abuja, Nigeria
- Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Institute of Epidemiology, Neuherberg, Germany
| | - Daudi Jjingo
- African Center of Excellence in Bioinformatics and Data-Intensive Sciences, Kampala, Uganda
- Department of Computer Science, Makerere University, Kampala, Uganda
- Infectious Diseases Institute, Kampala, Uganda
| | - David Kateete
- Department of Immunology and Molecular Biology, School of Biomedical Sciences, Makerere University College of Health Sciences, Kampala, Uganda
| | - Oyekanmi Nash
- Centre for Genomics Research and Innovation, NABDA/FMST, Abuja, Nigeria
| | - Dorothea Nitsch
- Department of Non-Communicable Disease Epidemiology, London School of Hygiene and Tropical Medicine, London School of Hygiene and Tropical Medicine, United Kingdom
| | - Moffat Nyirenda
- Department of Non-Communicable Disease Epidemiology, London School of Hygiene and Tropical Medicine, London School of Hygiene and Tropical Medicine, United Kingdom
- MRC/UVRI and LSHTM Uganda Research Unit, Entebbe, Uganda
| | - Dipender Gill
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, United Kingdom
| | - Eleftheria Zeggini
- Institute of Translational Genomics, Helmholtz Zentrum München – German Research Center for Environmental Health, Neuherberg, Germany
- TUM School of Medicine, Technical University of Munich and Klinikum Rechts der Isar, Munich, Germany
| | - Harald Grallert
- Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Institute of Epidemiology, Neuherberg, Germany
- German Center for Diabetes Research (DZD), München-Neuherberg, Neuherberg, Germany
| | - Annette Peters
- Helmholtz Zentrum München, German Research Center for Environmental Health (GmbH), Institute of Epidemiology, Neuherberg, Germany
- German Center for Diabetes Research (DZD), München-Neuherberg, Neuherberg, Germany
- Chair of Epidemiology, Institute for Medical Information Processing, Biometry and Epidemiology, Medical Faculty, Ludwig-Maximilians-Universität München, Munich, Germany
| | - Tinashe Chikowore
- Department of Medicine, Brigham and Women’s Hospital, Harvard Medical School Boston, Boston, MA, United States
- Wits Donald Gordon Medical Centre, School of Clinical Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa
| | - Chiara Batini
- Department of Population Health Sciences, University of Leicester, Leicester, United Kingdom
- University Hospitals of Leicester NHS Trust, Leicester, United Kingdom
| | - Opeyemi Soremekun
- Institute of Translational Genomics, Helmholtz Zentrum München – German Research Center for Environmental Health, Neuherberg, Germany
- Molecular Bio-computation and Drug Design Laboratory, School of Health Sciences, University of KwaZulu-Natal, Durban, South Africa
| | - Segun Fatumo
- The African Computational Genomics (TACG) Research Group, MRC/UVRI and LSHTM Uganda Research Unit, Entebbe, Uganda
- Precision Healthcare University Research Institute, Queen Mary University of London, United Kingdom
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6
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Hong H, Fu Q, Gu P, Zhao J, Dai J, Xu K, Yang T, Dai H, Shen S. Investigating the common genetic architecture and causality of metabolic disorders with neurodegenerative diseases. Diabetes Obes Metab 2025; 27:1337-1349. [PMID: 39703124 DOI: 10.1111/dom.16130] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 08/26/2024] [Revised: 12/03/2024] [Accepted: 12/03/2024] [Indexed: 12/21/2024]
Abstract
BACKGROUND The co-occurrence of metabolic dysfunction and neurodegenerative diseases suggests a genetic link, yet the shared genetic architecture and causality remain unclear. We aimed to comprehensively characterise these genetic relationships. METHODS We investigated genetic correlations among four neurodegenerative diseases and seven metabolic dysfunctions, followed by bidirectional Mendelian randomisation (MR) to assess potential causal relationships. Pleiotropy analysis (PLACO) was used to detect the pleiotropic effects of genetic variants. Significant pleiotropic loci were refined and annotated using functional mapping and annotation (FUMA) and Bayesian colocalisation analysis. We further explored mapped genes with tissue-specific expression and gene set enrichment analyses. RESULTS We identified significant genetic correlations in nine out of 28 trait pairs. MR suggested causal relationships between specific trait pairs. Pleiotropy analysis revealed 25 931 significant single-nucleotide polymorphisms, with 246 pleiotropic loci identified via FUMA and 55 causal loci through Bayesian colocalisation. These loci are involved in neurotransmitter transport and immune response mechanisms, notably the missense variant rs41286192 in SLC18B1. The tissue-specific analysis highlighted the pancreas, left ventricle, amygdala, and liver as critical organs in disease progression. Drug target analysis linked 74 unique genes to existing therapeutic agents, while gene set enrichment identified 189 pathways related to lipid metabolism, cell differentiation and immune responses. CONCLUSION Our findings reveal a shared genetic basis, pleiotropic loci, and potential causal relationships between metabolic dysfunction and neurodegenerative diseases. These insights highlight the biological connections underlying their phenotypic association and offer implications for future research to reduce the risk of neurodegenerative diseases.
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Affiliation(s)
- Hao Hong
- Department of Biostatistics, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China
| | - Qi Fu
- Department of Endocrinology and Metabolism, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China
| | - Pan Gu
- Department of Biostatistics, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China
| | - Jingyi Zhao
- Department of Biostatistics, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China
| | - Jinglan Dai
- Department of Biostatistics, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China
| | - Kuanfeng Xu
- Department of Endocrinology and Metabolism, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China
| | - Tao Yang
- Department of Endocrinology and Metabolism, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China
| | - Hao Dai
- Department of Endocrinology and Metabolism, the First Affiliated Hospital of Nanjing Medical University, Nanjing, China
| | - Sipeng Shen
- Department of Biostatistics, Center for Global Health, School of Public Health, Nanjing Medical University, Nanjing, China
- Jiangsu Key Lab of Cancer Biomarkers, Prevention and Treatment, Jiangsu Collaborative Innovation Center for Cancer Personalized Medicine, Nanjing Medical University, Nanjing, China
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Alagha M, Al-Alam F, Saroufine K, Elias L, Klaimi M, Nabbout G, Harb F, Azar S, Nahas N, Ghadieh HE. Binge Eating Disorder and Metabolic Syndrome: Shared Mechanisms and Clinical Implications. Healthcare (Basel) 2025; 13:482. [PMID: 40077044 PMCID: PMC11898466 DOI: 10.3390/healthcare13050482] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/12/2025] [Revised: 02/14/2025] [Accepted: 02/21/2025] [Indexed: 03/14/2025] Open
Abstract
Background: Binge eating disorder (BED) is characterized by episodes of uncontrollable eating, defined by the rapid consumption of large quantities of food over a short period. This condition is associated with a variety of psychological and non-psychological factors, including behavioral, biological, genetic, neurological, and pharmacological influences, all of which adversely affect patients' daily lives. BED is linked to numerous health consequences, such as obesity, atherosclerosis, diabetes, chronic pain, and hypertension. Although BED is not exclusive to individuals with obesity, it is more prevalent in this population, who also face a heightened risk of developing metabolic syndrome (MetS). The latter is a cluster of five risk factors-obesity, hyperlipidemia, hyperinsulinemia, hypertension, and hyperglycemia-that significantly increase the likelihood of chronic diseases. Methods: This narrative review synthesizes existing research to explore the association between BED and MetS, examining shared pathophysiological mechanisms and clinical implications. It also highlights the role of escalating food insecurity and ongoing political, economic, and health crises in the development of BED. Results: BED is significantly associated with MetS components, including hypertension, obesity, type 2 diabetes, and dyslipidemia, all contributing to increased morbidity and mortality. Beyond body weight, behavioral, genetic, biological, and neurological factors mediate this relationship. Conclusions: BED is strongly linked to MetS through shared behavioral, genetic, and biological pathways. Early detection, integrated management strategies, and further research are crucial to addressing the public health challenges posed by this association.
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Affiliation(s)
- Michel Alagha
- Department of Biomedical Sciences, Faculty of Medicine and Medical Sciences, University of Balamand, Al-Koura, Tripoli P.O. Box 100, Lebanon; (M.A.); (K.S.); (L.E.); (G.N.); (F.H.); (S.A.)
| | - Firas Al-Alam
- Department of Psychology, Faculty of Arts and Sciences, University of Balamand, Al-Koura, Tripoli P.O. Box 100, Lebanon; (F.A.-A.); (N.N.)
| | - Karmen Saroufine
- Department of Biomedical Sciences, Faculty of Medicine and Medical Sciences, University of Balamand, Al-Koura, Tripoli P.O. Box 100, Lebanon; (M.A.); (K.S.); (L.E.); (G.N.); (F.H.); (S.A.)
| | - Linda Elias
- Department of Biomedical Sciences, Faculty of Medicine and Medical Sciences, University of Balamand, Al-Koura, Tripoli P.O. Box 100, Lebanon; (M.A.); (K.S.); (L.E.); (G.N.); (F.H.); (S.A.)
| | - Mark Klaimi
- Department of Biology, Faculty of Arts and Sciences, University of Balamand, Al-Koura, Tripoli P.O. Box 100, Lebanon;
| | - Ghassan Nabbout
- Department of Biomedical Sciences, Faculty of Medicine and Medical Sciences, University of Balamand, Al-Koura, Tripoli P.O. Box 100, Lebanon; (M.A.); (K.S.); (L.E.); (G.N.); (F.H.); (S.A.)
| | - Frederic Harb
- Department of Biomedical Sciences, Faculty of Medicine and Medical Sciences, University of Balamand, Al-Koura, Tripoli P.O. Box 100, Lebanon; (M.A.); (K.S.); (L.E.); (G.N.); (F.H.); (S.A.)
| | - Sami Azar
- Department of Biomedical Sciences, Faculty of Medicine and Medical Sciences, University of Balamand, Al-Koura, Tripoli P.O. Box 100, Lebanon; (M.A.); (K.S.); (L.E.); (G.N.); (F.H.); (S.A.)
| | - Nayla Nahas
- Department of Psychology, Faculty of Arts and Sciences, University of Balamand, Al-Koura, Tripoli P.O. Box 100, Lebanon; (F.A.-A.); (N.N.)
| | - Hilda E. Ghadieh
- Department of Biomedical Sciences, Faculty of Medicine and Medical Sciences, University of Balamand, Al-Koura, Tripoli P.O. Box 100, Lebanon; (M.A.); (K.S.); (L.E.); (G.N.); (F.H.); (S.A.)
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8
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Dhamija R, Tewari S, Gill PS, Monga N, Mittal S, Duhan J. Association of Apical Periodontitis with Glycated Hemoglobin Levels and Systemic Inflammatory Markers in Patients with Type 2 Diabetes: A Cross-Sectional Study. J Endod 2025; 51:124-131. [PMID: 39581537 DOI: 10.1016/j.joen.2024.11.008] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/13/2024] [Revised: 10/22/2024] [Accepted: 11/14/2024] [Indexed: 11/26/2024]
Abstract
INTRODUCTION This cross-sectional study, as a preliminary part of an ongoing project, aimed to investigate the effect of apical peridontitis (AP) on glycated hemoglobin (HbA1c) and systemic inflammatory markers in diabetic individuals. METHODS A total of 280 individuals (140 with type 2 diabetes mellitus [T2DM] and 140 healthy) with and without AP were enrolled. Sixty-four age-, gender-, and body mass index-matched participants each in T2DM with AP group (DAP), T2DM without apical periodontitis (D), systemically healthy controls with apical periodontitis (CAP), and without apical periodontitis (C) groups were evaluated. Radiologic and clinical oral examination was performed for confirming the diagnosis of AP and periapical index scoring (PAI). Blood analyses were carried out for interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF)-α, high-sensitivity C-reactive protein (hsCRP), and HbA1c assessment. RESULTS Significantly higher levels of IL-1β, TNF-α, and hsCRP were observed in patients with AP in both diabetes and control groups (P < .05). In the diabetes group, AP contributed to significantly raised levels of HbA1c compared with T2DM group patients without AP. After controlling for possible confounders, partial corelation coefficients revealed positive corelation of presence of AP as well as size of the periapical lesion with HbA1c and serum levels of inflammatory markers in both diabetic and healthy individuals. Multivariate linear regression analysis revealed both presence of AP (P < .05) as well as the size of lesion (P < .001) were found to significantly predict the HbA1c levels as well as the levels of IL-1β, IL-6, TNF-α, and hsCRP in both diabetic and non-diabetic individuals. CONCLUSIONS These findings suggest that both presence of AP and size of periapical lesion was associated with glycemic control and systemic inflammatory burden in patients with T2DM.
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Affiliation(s)
- Ritika Dhamija
- Department of Conservative Dentistry and Endodontics, Post Graduate Institute of Dental Sciences, Rohtak, Haryana, India
| | - Sanjay Tewari
- Department of Conservative Dentistry and Endodontics, Post Graduate Institute of Dental Sciences, Rohtak, Haryana, India.
| | - Paramjeet Singh Gill
- Department of Microbiology, Post Graduate Institute of Medical Sciences, Rohtak, Haryana, India
| | - Nitika Monga
- Division of Development Research, Indian Council of Medical Research, New Delhi, India
| | - Shweta Mittal
- Department of Conservative Dentistry and Endodontics, Post Graduate Institute of Dental Sciences, Rohtak, Haryana, India
| | - Jigyasa Duhan
- Department of Conservative Dentistry and Endodontics, Post Graduate Institute of Dental Sciences, Rohtak, Haryana, India
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9
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Amato M, Polizzi A, Viglianisi G, Leonforte F, Mascitti M, Isola G. Impact of Periodontitis and Oral Dysbiosis Metabolites in the Modulation of Accelerating Ageing and Human Senescence. Metabolites 2025; 15:35. [PMID: 39852378 PMCID: PMC11767177 DOI: 10.3390/metabo15010035] [Citation(s) in RCA: 2] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/24/2024] [Revised: 01/03/2025] [Accepted: 01/08/2025] [Indexed: 01/26/2025] Open
Abstract
Periodontitis, a chronic multifactorial inflammatory condition of the periodontium, is originated by a dysbiotic oral microbiota and is negatively correlated with several systemic diseases. The low-chronic burden of gingival inflammation not only exacerbates periodontitis but also predisposes individuals to a spectrum of age-related conditions, including cardiovascular diseases, neurodegenerative disorders, and metabolic dysfunction, especially related to ageing. In this regard, over the local periodontal treatment, lifestyle modifications and adjunctive therapies may offer synergistic benefits in ameliorating both oral and systemic health in ageing populations. Elucidating the intricate connections between periodontitis and senescence is important for understanding oral health's systemic implications for ageing and age-related diseases. Effective management strategies targeting the oral microbiota and senescent pathways may offer novel avenues for promoting healthy ageing and preventing age-related morbidities. This review will analyze the current literature about the intricate interplay between periodontitis, oral dysbiosis, and the processes of senescence, shedding light on their collective impact on the modulation and accelerated ageing and age-related diseases. Lastly, therapeutic strategies targeting periodontitis and oral dysbiosis to mitigate senescence and its associated morbidities will be discussed.
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Affiliation(s)
- Mariacristina Amato
- Department of General Surgery and Surgical-Medical Specialties, School of Dentistry, University of Catania, 95124 Catania, Italy
| | - Alessandro Polizzi
- Department of General Surgery and Surgical-Medical Specialties, School of Dentistry, University of Catania, 95124 Catania, Italy
| | - Gaia Viglianisi
- Department of General Surgery and Surgical-Medical Specialties, School of Dentistry, University of Catania, 95124 Catania, Italy
| | - Francesco Leonforte
- Hygiene Unit, Department of Medical and Surgical Sciences and Advanced Technologies, University of Catania, 95124 Catania, Italy
| | - Marco Mascitti
- Department of Clinical Specialistic and Dental Sciences, Marche Polytechnic University, 60121 Ancona, Italy
| | - Gaetano Isola
- Department of General Surgery and Surgical-Medical Specialties, School of Dentistry, University of Catania, 95124 Catania, Italy
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10
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Le TN, Bright R, Truong V, Li J, Juneja R, Vasilev K. Key biomarkers in type 2 diabetes patients: A systematic review. Diabetes Obes Metab 2025; 27:7-22. [PMID: 39355932 PMCID: PMC11618249 DOI: 10.1111/dom.15991] [Citation(s) in RCA: 5] [Impact Index Per Article: 5.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/23/2024] [Revised: 09/10/2024] [Accepted: 09/19/2024] [Indexed: 10/03/2024]
Abstract
Type 2 diabetes mellitus (T2DM) is not just a local health issue but a significant global health burden, affecting patient outcomes and clinical management worldwide. Despite the wealth of studies reporting T2DM biomarkers, there is an urgent need for a comparative review. This review aims to provide a comprehensive analysis based on the reported T2DM biomarkers and how these are linked with other conditions, such as inflammation and wound healing. A comparative review was conducted on 24 001 study participants, including 10 024 T2DM patients and 13 977 controls (CTL; age 30-90 years). Four main profiles were extracted and analysed from the clinical reports over the past 11 years: haematological (1084 cases vs. 1458 CTL), protein (6753 cases vs. 9613 CTL), cytokine (975 cases vs. 1350 CTL) and lipid (1212 cases vs. 1556 CTL). This review provides a detailed analysis of the haematological profile in T2DM patients, highlighting fundamental changes such as increased white blood cells and platelet counts, accompanied by decreases in red blood cell counts and iron absorption. In the serum protein profile, a reduction in albumin and anti-inflammatory cytokines was noted along with an increase in globulin levels and pro-inflammatory cytokines. Furthermore, changes in lipid profiles were discussed, specifically the decreases in high-density lipoprotein (HDL) and the increases in low-density lipoprotein (LDL) and triglycerides. Understanding the changes in these four biomarker profiles is essential for developing innovative strategies to create diagnostic and prognostic tools for diabetes management.
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Affiliation(s)
- Thien Ngoc Le
- College of Medicine and Public HealthFlinders UniversityAdelaideSouth AustraliaAustralia
| | - Richard Bright
- College of Medicine and Public HealthFlinders UniversityAdelaideSouth AustraliaAustralia
| | - Vi‐Khanh Truong
- College of Medicine and Public HealthFlinders UniversityAdelaideSouth AustraliaAustralia
| | - Jordan Li
- College of Medicine and Public HealthFlinders UniversityAdelaideSouth AustraliaAustralia
- Department of Renal Medicine, Flinders Medical CentreBedford ParkSouth AustraliaAustralia
| | - Rajiv Juneja
- College of Medicine and Public HealthFlinders UniversityAdelaideSouth AustraliaAustralia
- Department of Renal Medicine, Flinders Medical CentreBedford ParkSouth AustraliaAustralia
| | - Krasimir Vasilev
- College of Medicine and Public HealthFlinders UniversityAdelaideSouth AustraliaAustralia
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11
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Lin Y, Cheng L, Chen Y, Li W, Guo Q, Miao Y. TFEB signaling promotes autophagic degradation of NLRP3 to attenuate neuroinflammation in diabetic encephalopathy. Am J Physiol Cell Physiol 2024; 327:C1481-C1496. [PMID: 39437446 DOI: 10.1152/ajpcell.00322.2024] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/14/2024] [Revised: 09/18/2024] [Accepted: 10/02/2024] [Indexed: 10/25/2024]
Abstract
Diabetic encephalopathy (DE), a neurological complication of diabetes mellitus, has an unclear etiology. Shreds of evidence show that the nucleotide-binding oligomerization domain-like receptor family protein 3 (NLRP3) inflammasome-induced neuroinflammation and transcription factor EB (TFEB)-mediated autophagy impairment may take part in DE development. The cross talk between these two pathways and their contribution to DE remains to be explored. A mouse model of type 2 diabetes mellitus (T2DM) exhibiting cognitive dysfunction was created, along with high-glucose (HG) cultured BV2 cells. Following, 3-methyladenine (3-MA) and rapamycin were used to modulate autophagy. To evaluate the potential therapeutic benefits of TFEB in DE, we overexpressed and knocked down TFEB in both mice and cells. Autophagy impairment and NLRP3 inflammasome activation were noticed in T2DM mice and HG-cultured BV2 cells. The inflammatory response caused by NLRP3 inflammasome activation was decreased by rapamycin-induced autophagy enhancement, while 3-MA treatment further deteriorated it. Nuclear translocation and expression of TFEB were hampered in HG-cultured BV2 cells and T2DM mice. Exogenous TFEB overexpression boosted NLRP3 degradation via autophagy, which in turn alleviated microglial activation as well as ameliorated cognitive deficits and neuronal damage. In addition, TFEB knockdown exacerbated neuroinflammation by decreasing autophagy-mediated NLRP3 degradation. Our findings have unraveled the pathogenesis of a previously underappreciated disease, implying that the activation of NLRP3 inflammasome and impairment of autophagy in microglia are significant etiological factors in the DE. The TFEB-mediated autophagy pathway can reduce neuroinflammation by enhancing NLRP3 degradation. This could potentially serve as a viable and innovative treatment approach for DE.NEW & NOTEWORTHY This article delves into the intricate connections between inflammation, autophagy, diabetes, and neurodegeneration, with a particular focus on a disease that is not yet fully understood-diabetic encephalopathy (DE). TFEB emerges as a pivotal regulator in balancing autophagy and inflammation in DE. Our findings highlight the crucial function of the TFEB-mediated autophagy pathway in mitigating inflammatory damage in DE, suggesting a new treatment strategy.
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Affiliation(s)
- Yijia Lin
- Department of Geriatrics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
| | - Lizhen Cheng
- Department of Geriatrics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
| | - Yixin Chen
- Department of Geriatrics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
| | - Wei Li
- Department of Geriatrics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
| | - Qihao Guo
- Department of Geriatrics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
| | - Ya Miao
- Department of Geriatrics, Shanghai Sixth People's Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China
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12
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Zhang M, Ye S, Li J, Zhang M, Tan L, Wang Y, Xie P, Peng H, Li S, Chen S, Wen Q, Chan KW, Tang SCW, Li B, Chen W. Association of systemic immune-inflammation index with all-cause and cardio-cerebrovascular mortality in individuals with diabetic kidney disease: evidence from NHANES 1999-2018. Front Endocrinol (Lausanne) 2024; 15:1399832. [PMID: 39659615 PMCID: PMC11628304 DOI: 10.3389/fendo.2024.1399832] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/12/2024] [Accepted: 11/11/2024] [Indexed: 12/12/2024] Open
Abstract
Background Emerging evidence suggests a potential role of immune response and inflammation in the pathogenesis of diabetic kidney disease (DKD). The systemic immune-inflammation index (SII) offers a comprehensive measure of inflammation; however, its relationship with the prognosis of DKD patients remains unclear. Methods Using data from the National Health and Nutrition Examination Survey (NHANES) spanning 1999 to 2018, this cross-sectional study involved adults diagnosed with DKD. Cox proportional hazards models were utilized to assess the associations between SII and all-cause or cardio-cerebrovascular disease mortality. Additionally, restricted cubic spline, piecewise linear regression, and subgroup analyses were performed. Results Over a median follow-up duration of 6.16 years, 1338 all-cause deaths were recorded. After adjusting for covariates, elevated SII levels were significantly associated with increased risks of all-cause and cardio-cerebrovascular disease mortality. Specifically, per one-unit increment in natural log-transformed SII (lnSII), there was a 29% increased risk of all-cause mortality (P < 0.001) and a 23% increased risk of cardio-cerebrovascular disease mortality (P = 0.01) in the fully adjusted model. Similar results were observed when SII was analyzed as a categorical variable (quartiles). Moreover, nonlinear association was identified between SII and all-cause mortality (P < 0.001) through restricted cubic spline analysis, with threshold value of 5.82 for lnSII. The robustness of these findings was confirmed in subgroup analyses. Likewise, the statistically significant correlation between SII levels and cardio-cerebrovascular disease mortality persisted in individuals with DKD. Conclusion Increased SII levels, whether examined as continuous variables or categorized, demonstrate a significant association with elevated risks of all-cause and cardio-cerebrovascular disease mortality among DKD patients. These findings imply that maintaining SII within an optimal range could be crucial in reducing mortality risk.
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Affiliation(s)
- Manhuai Zhang
- Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
- National Health Commission (NHC) Key Laboratory of Clinical Nephrology (Sun Yat-sen University) and Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, China
| | - Siyang Ye
- Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
- National Health Commission (NHC) Key Laboratory of Clinical Nephrology (Sun Yat-sen University) and Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, China
| | - Jianbo Li
- Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
- National Health Commission (NHC) Key Laboratory of Clinical Nephrology (Sun Yat-sen University) and Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, China
| | - Meng Zhang
- Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
- National Health Commission (NHC) Key Laboratory of Clinical Nephrology (Sun Yat-sen University) and Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, China
| | - Li Tan
- Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
- National Health Commission (NHC) Key Laboratory of Clinical Nephrology (Sun Yat-sen University) and Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, China
| | - Yiqin Wang
- Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
- National Health Commission (NHC) Key Laboratory of Clinical Nephrology (Sun Yat-sen University) and Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, China
| | - Peichen Xie
- Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
- National Health Commission (NHC) Key Laboratory of Clinical Nephrology (Sun Yat-sen University) and Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, China
| | - Huajing Peng
- Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
- National Health Commission (NHC) Key Laboratory of Clinical Nephrology (Sun Yat-sen University) and Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, China
| | - Suchun Li
- Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
- National Health Commission (NHC) Key Laboratory of Clinical Nephrology (Sun Yat-sen University) and Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, China
| | - Sixiu Chen
- Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
- National Health Commission (NHC) Key Laboratory of Clinical Nephrology (Sun Yat-sen University) and Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, China
| | - Qiong Wen
- Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
- National Health Commission (NHC) Key Laboratory of Clinical Nephrology (Sun Yat-sen University) and Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, China
| | - Kam Wa Chan
- School of Chinese Medicine, Hong Kong Baptist University, Hong Kong, Hong Kong SAR, China
| | - Sydney C. W. Tang
- Division of Nephrology, Department of Medicine, LKS Faculty of Medicine, The University of Hong Kong, Hong Kong, Hong Kong SAR, China
| | - Bin Li
- Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
- National Health Commission (NHC) Key Laboratory of Clinical Nephrology (Sun Yat-sen University) and Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, China
| | - Wei Chen
- Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China
- National Health Commission (NHC) Key Laboratory of Clinical Nephrology (Sun Yat-sen University) and Guangdong Provincial Key Laboratory of Nephrology, Guangzhou, China
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13
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Zhang S, Wu Y, Mprah R, Wang M. COVID-19 and persistent symptoms: implications for polycystic ovary syndrome and its management. Front Endocrinol (Lausanne) 2024; 15:1434331. [PMID: 39429741 PMCID: PMC11486749 DOI: 10.3389/fendo.2024.1434331] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 05/17/2024] [Accepted: 08/28/2024] [Indexed: 10/22/2024] Open
Abstract
The COVID-19 pandemic has left a profound mark on global health, leading to substantial morbidity and mortality worldwide. Beyond the immediate symptoms of infection, the emergence of "long COVID", the long-term effects of SARS-CoV-2, has become a significant public health concern. Long COVID is a multifaceted condition affecting various organs and systems, including the cardiovascular, digestive, nervous, and endocrine systems. Individuals diagnosed with polycystic ovary syndrome (PCOS) may face an increased risk of severe COVID-19 symptoms and infection. It is crucial to comprehend how long COVID affects PCOS patients to devise effective treatment and care strategies. Here, we review the detrimental effects of COVID-19 and its long-term effects on reproductive health, endocrine function, inflammation, metabolism, cardiovascular health, body composition, lifestyle, and mental health in patients with PCOS. We offer recommendations for the post-covid-19 management of PCOS, emphasizing the necessity of a comprehensive, multidisciplinary approach to patient care. Furthermore, we discuss prospective research directions, highlighting the significance of continued investigations and clinical trials to evaluate treatment approaches for long COVID and its ramifications in individuals with PCOS.
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Affiliation(s)
- Shanshan Zhang
- School of Biological Science, Jining Medical University, Rizhao, Shandong, China
| | - Yanqun Wu
- School of Biological Science, Jining Medical University, Rizhao, Shandong, China
| | - Richard Mprah
- Department of Physiology, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou, Jiangsu, China
| | - Mingming Wang
- Department of Physiology, School of Basic Medical Sciences, Xuzhou Medical University, Xuzhou, Jiangsu, China
- China National Experimental Teaching Demonstration Center for Basic Medicine, Xuzhou Medical University, Xuzhou, Jiangsu, China
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14
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Tran DQ, Nguyen Di K, Quynh Chi VT, Nguyen HTH. Evaluating the effects of dietary patterns on circulating C-reactive protein levels in the general adult population: an umbrella review of meta-analyses of interventional and observational studies. Br J Nutr 2024; 132:783-793. [PMID: 39364652 DOI: 10.1017/s0007114524001648] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 10/05/2024]
Abstract
Adopting a healthy dietary pattern may be an initial step in combating inflammation-related chronic diseases; however, a comprehensive synthesis evaluating current evidence is lacking. This umbrella review aimed to summarise the current evidence on the effects of dietary patterns on circulating C-reactive protein (CRP) levels in adults. We conducted an exhaustive search of the Pubmed, Scopus and Epistemonikos databases, spanning from their inception to November 2023, to identify systematic reviews and meta-analyses across all study designs. Subsequently, we employed a random-effects model to recompute the pooled mean difference. Methodological quality was assessed using the A Measurement Tool to Assess Systematic Reviews 2 (AMSTAR 2) checklist, and evidence certainty was categorised as non-significant, weak, suggestive, highly suggestive or convincing (PROSPERO: CRD42023484917). We included twenty-seven articles with thirty meta-analyses of seven dietary patterns, fifteen of which (50 %) exhibited high methodological quality. The summary effects of randomised controlled trials (RCT) found that the Mediterranean diet was the most effective in reducing circulating CRP levels, followed by Vegetarian/Vegan and Energy-restricted diets, though the evidence was of weak quality. In contrast, Intermittent Fasting, Ketogenic, Nordic and Paleolithic diets did not show an inverse correlation with circulating CRP levels. Some results from combined interventional and observational studies, as well as solely observational studies, also agreed with these findings. These dietary patterns show the potential in reducing CRP levels in adults, yet the lack of high-quality evidence suggests future studies may alter the summary estimates. Therefore, further well-conducted studies are warranted.
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Affiliation(s)
- Duc Quang Tran
- Faculty of Technology, Dong Nai Technology University, Bien Hoa City, Vietnam
| | - Khanh Nguyen Di
- Faculty of Technology, Dong Nai Technology University, Bien Hoa City, Vietnam
| | - Vu Thi Quynh Chi
- The University of Danang - School of Medicine and Pharmacy, Danang550000, Vietnam
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15
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Sinha SK, Carpio MB, Nicholas SB. Fiery Connections: Macrophage-Mediated Inflammation, the Journey from Obesity to Type 2 Diabetes Mellitus and Diabetic Kidney Disease. Biomedicines 2024; 12:2209. [PMID: 39457523 PMCID: PMC11503991 DOI: 10.3390/biomedicines12102209] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/15/2024] [Revised: 09/12/2024] [Accepted: 09/23/2024] [Indexed: 10/28/2024] Open
Abstract
The high prevalence of diabetes mellitus (DM) poses a significant public health challenge, with diabetic kidney disease (DKD) as one of its most serious consequences. It has become increasingly clear that type 2 DM (T2D) and the complications of DKD are not purely metabolic disorders. This review outlines emerging evidence related to the step-by-step contribution of macrophages to the development and progression of DKD in individuals who specifically develop T2D as a result of obesity. The macrophage is a prominent inflammatory cell that contributes to obesity, where adipocyte hypertrophy leads to macrophage recruitment and eventually to the expansion of adipose tissue. The recruited macrophages secrete proinflammatory cytokines, which cause systemic inflammation, glucose dysregulation, and insulin sensitivity, ultimately contributing to the development of T2D. Under such pathological changes, the kidney is susceptible to elevated glucose and thereby activates signaling pathways that ultimately drive monocyte recruitment. In particular, the early recruitment of proinflammatory macrophages in the diabetic kidney produces inflammatory cytokines/chemokines that contribute to inflammation and tissue damage associated with DKD pathology. Macrophage activation and recruitment are crucial inciting factors that also persist as DKD progresses. Thus, targeting macrophage activation and function could be a promising therapeutic approach, potentially offering significant benefits for managing DKD at all stages of progression.
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Affiliation(s)
- Satyesh K. Sinha
- Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA;
- Department of Internal Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA 90059, USA
| | - Maria Beatriz Carpio
- Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA;
| | - Susanne B. Nicholas
- Department of Medicine, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA;
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16
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Brito Nunes C, Borges MC, Freathy RM, Lawlor DA, Qvigstad E, Evans DM, Moen GH. Understanding the Genetic Landscape of Gestational Diabetes: Insights into the Causes and Consequences of Elevated Glucose Levels in Pregnancy. Metabolites 2024; 14:508. [PMID: 39330515 PMCID: PMC11434570 DOI: 10.3390/metabo14090508] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/26/2024] [Revised: 09/16/2024] [Accepted: 09/17/2024] [Indexed: 09/28/2024] Open
Abstract
Background/Objectives: During pregnancy, physiological changes in maternal circulating glucose levels and its metabolism are essential to meet maternal and fetal energy demands. Major changes in glucose metabolism occur throughout pregnancy and consist of higher insulin resistance and a compensatory increase in insulin secretion to maintain glucose homeostasis. For some women, this change is insufficient to maintain normoglycemia, leading to gestational diabetes mellitus (GDM), a condition characterized by maternal glucose intolerance and hyperglycaemia first diagnosed during the second or third trimester of pregnancy. GDM is diagnosed in approximately 14.0% of pregnancies globally, and it is often associated with short- and long-term adverse health outcomes in both mothers and offspring. Although recent studies have highlighted the role of genetic determinants in the development of GDM, research in this area is still lacking, hindering the development of prevention and treatment strategies. Methods: In this paper, we review recent advances in the understanding of genetic determinants of GDM and glycaemic traits during pregnancy. Results/Conclusions: Our review highlights the need for further collaborative efforts as well as larger and more diverse genotyped pregnancy cohorts to deepen our understanding of the genetic aetiology of GDM, address research gaps, and further improve diagnostic and treatment strategies.
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Affiliation(s)
- Caroline Brito Nunes
- Institute for Molecular Bioscience, The University of Queensland, Brisbane 4067, Australia
| | - Maria Carolina Borges
- MRC Integrative Epidemiology Unit, University of Bristol, Bristol BS8 1QU, UK
- Population Health Sciences, Bristol Medical School, University of Bristol, Bristol BS8 2PS, UK
| | - Rachel M. Freathy
- Department of Clinical and Biomedical Sciences, Faculty of Health and Life Sciences, University of Exeter, Exeter EX4 4PY, UK;
| | - Deborah A. Lawlor
- MRC Integrative Epidemiology Unit, University of Bristol, Bristol BS8 1QU, UK
- Population Health Sciences, Bristol Medical School, University of Bristol, Bristol BS8 2PS, UK
| | - Elisabeth Qvigstad
- Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, 0372 Oslo, Norway
- Department of Endocrinology, Morbid Obesity and Preventive Medicine, Oslo University Hospital, 0424 Oslo, Norway
| | - David M. Evans
- Institute for Molecular Bioscience, The University of Queensland, Brisbane 4067, Australia
- MRC Integrative Epidemiology Unit, University of Bristol, Bristol BS8 1QU, UK
- Frazer Institute, University of Queensland, Brisbane 4102, Australia
| | - Gunn-Helen Moen
- Institute for Molecular Bioscience, The University of Queensland, Brisbane 4067, Australia
- Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, 0372 Oslo, Norway
- Frazer Institute, University of Queensland, Brisbane 4102, Australia
- K.G. Jebsen Center for Genetic Epidemiology, Department of Public Health and Nursing, NTNU, Norwegian University of Science and Technology, 7491 Trondheim, Norway
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17
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Nakanishi Y, Izumi M, Matsushita H, Koyama Y, Diez D, Takamatsu H, Koyama S, Nishide M, Naito M, Mizuno Y, Yamaguchi Y, Mae T, Noda Y, Nakaya K, Nojima S, Sugihara F, Okuzaki D, Ikawa M, Shimada S, Kang S, Kumanogoh A. Semaphorin 6D tunes amygdalar circuits for emotional, metabolic, and inflammatory outputs. Neuron 2024; 112:2955-2972.e9. [PMID: 39002542 DOI: 10.1016/j.neuron.2024.06.017] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/06/2023] [Revised: 04/20/2024] [Accepted: 06/19/2024] [Indexed: 07/15/2024]
Abstract
Regulated neural-metabolic-inflammatory responses are essential for maintaining physiological homeostasis. However, the molecular machinery that coordinates neural, metabolic, and inflammatory responses is largely unknown. Here, we show that semaphorin 6D (SEMA6D) coordinates anxiogenic, metabolic, and inflammatory outputs from the amygdala by maintaining synaptic homeostasis. Using genome-wide approaches, we identify SEMA6D as a pleiotropic gene for both psychiatric and metabolic traits in human. Sema6d deficiency increases anxiety in mice. When fed a high-fat diet, Sema6d-/- mice display attenuated obesity and enhanced myelopoiesis compared with control mice due to higher sympathetic activity via the β3-adrenergic receptor. Genetic manipulation and spatial and single-nucleus transcriptomics reveal that SEMA6D in amygdalar interneurons is responsible for regulating anxiogenic and autonomic responses. Mechanistically, SEMA6D is required for synaptic maturation and γ-aminobutyric acid transmission. These results demonstrate that SEMA6D is important for the normal functioning of the neural circuits in the amygdala, coupling emotional, metabolic, and inflammatory responses.
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Affiliation(s)
- Yoshimitsu Nakanishi
- Department of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan; Department of Immunopathology, World Premier International Research Center Initiative Immunology Frontier Research Center (WPI-IFReC), Osaka University, Osaka 565-0871, Japan; Department of Advanced Clinical and Translational Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan; Integrated Frontier Research for Medical Science Division, Institute for Open and Transdisciplinary Research Initiatives (OTRI), Osaka University, Osaka 565-0871, Japan
| | - Mayuko Izumi
- Department of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan; Department of Immunopathology, World Premier International Research Center Initiative Immunology Frontier Research Center (WPI-IFReC), Osaka University, Osaka 565-0871, Japan; Department of Advanced Clinical and Translational Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan; Integrated Frontier Research for Medical Science Division, Institute for Open and Transdisciplinary Research Initiatives (OTRI), Osaka University, Osaka 565-0871, Japan
| | - Hiroaki Matsushita
- Department of Advanced Clinical and Translational Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan; Discovery Pharmacology Department, Research Division, Chugai Pharmaceutical Co. Ltd., Kanagawa 247-8530, Japan
| | - Yoshihisa Koyama
- Integrated Frontier Research for Medical Science Division, Institute for Open and Transdisciplinary Research Initiatives (OTRI), Osaka University, Osaka 565-0871, Japan; Department of Neuroscience and Cell Biology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan; Addiction Research Unit, Osaka Psychiatric Research Center, Osaka Psychiatric Medical Center, Osaka 541-8567, Japan
| | - Diego Diez
- Quantitative Immunology Research Unit, WPI-IFReC, Osaka University, Osaka 565-0871, Japan
| | - Hyota Takamatsu
- Department of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan; Department of Immunopathology, World Premier International Research Center Initiative Immunology Frontier Research Center (WPI-IFReC), Osaka University, Osaka 565-0871, Japan
| | - Shohei Koyama
- Department of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan; Department of Immunopathology, World Premier International Research Center Initiative Immunology Frontier Research Center (WPI-IFReC), Osaka University, Osaka 565-0871, Japan
| | - Masayuki Nishide
- Department of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan; Department of Immunopathology, World Premier International Research Center Initiative Immunology Frontier Research Center (WPI-IFReC), Osaka University, Osaka 565-0871, Japan
| | - Maiko Naito
- Department of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan; Department of Immunopathology, World Premier International Research Center Initiative Immunology Frontier Research Center (WPI-IFReC), Osaka University, Osaka 565-0871, Japan
| | - Yumiko Mizuno
- Department of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan; Department of Immunopathology, World Premier International Research Center Initiative Immunology Frontier Research Center (WPI-IFReC), Osaka University, Osaka 565-0871, Japan
| | - Yuta Yamaguchi
- Department of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan; Department of Immunopathology, World Premier International Research Center Initiative Immunology Frontier Research Center (WPI-IFReC), Osaka University, Osaka 565-0871, Japan
| | - Tomoki Mae
- Department of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan
| | - Yu Noda
- Department of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan
| | - Kamon Nakaya
- Department of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan
| | - Satoshi Nojima
- Department of Pathology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan
| | - Fuminori Sugihara
- Laboratory of Biofunctional Imaging, WPI-IFReC, Osaka University, Osaka 565-0871, Japan
| | - Daisuke Okuzaki
- Integrated Frontier Research for Medical Science Division, Institute for Open and Transdisciplinary Research Initiatives (OTRI), Osaka University, Osaka 565-0871, Japan; Laboratory of Human Immunology (Single Cell Genomics), WPI-IFReC, Osaka University, Osaka 565-0871, Japan; Genome Information Research Center, Research Institute for Microbial Diseases (RIMD), Osaka University, Osaka 565-0871, Japan; Center for Infectious Diseases for Education and Research (CiDER), Osaka University, Osaka 565-0871, Japan; Japan Agency for Medical Research and Development-Core Research for Evolutional Science and Technology (AMED-CREST), Osaka University, Osaka 565-0871, Japan
| | - Masahito Ikawa
- Department of Experimental Genome Research, RIMD, Osaka University, Osaka 565-0871, Japan; Center for Infectious Diseases for Education and Research (CiDER), Osaka University, Osaka 565-0871, Japan; Center for Advanced Modalities and DDS (CAMaD), Osaka University, Osaka 565-0871, Japan
| | - Shoichi Shimada
- Department of Neuroscience and Cell Biology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan; Addiction Research Unit, Osaka Psychiatric Research Center, Osaka Psychiatric Medical Center, Osaka 541-8567, Japan
| | - Sujin Kang
- Laboratory of Immune Regulation, WPI-IFReC, Osaka University, Osaka 565-0871, Japan; Center for Infectious Diseases for Education and Research (CiDER), Osaka University, Osaka 565-0871, Japan.
| | - Atsushi Kumanogoh
- Department of Respiratory Medicine and Clinical Immunology, Graduate School of Medicine, Osaka University, Osaka 565-0871, Japan; Department of Immunopathology, World Premier International Research Center Initiative Immunology Frontier Research Center (WPI-IFReC), Osaka University, Osaka 565-0871, Japan; Integrated Frontier Research for Medical Science Division, Institute for Open and Transdisciplinary Research Initiatives (OTRI), Osaka University, Osaka 565-0871, Japan; Center for Infectious Diseases for Education and Research (CiDER), Osaka University, Osaka 565-0871, Japan; Japan Agency for Medical Research and Development-Core Research for Evolutional Science and Technology (AMED-CREST), Osaka University, Osaka 565-0871, Japan; Center for Advanced Modalities and DDS (CAMaD), Osaka University, Osaka 565-0871, Japan.
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18
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Adeli S, Maroofi M, Pourteymour Fard Tabrizi F, Alipour B, Heidari M, Vajdi M, Abbasalizad-Farhangi M. Effects of Propolis Consumption on Glycemic Indices and Liver Enzymes in Adults: A Grading of Recommendations Assessment, Development, and Valuation-assessed Systematic Review and Dose-Response Meta-analysis. Clin Ther 2024; 46:e6-e14. [PMID: 39097520 DOI: 10.1016/j.clinthera.2024.06.022] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/03/2024] [Revised: 06/20/2024] [Accepted: 06/28/2024] [Indexed: 08/05/2024]
Abstract
PURPOSE Even though various randomized controlled trials (RCTs) have assessed the effect of propolis on glycemic indices and liver enzyme concentrations in adults, results have been inconsistent, without conclusive evidence. This systematic review and meta-analysis of RCTs sought to evaluate the effects of propolis consumption on glycemic indices and liver enzymes, fasting blood glucose, insulin, homeostatic model assessment of insulin resistance, glycosylated hemoglobin, alanine transaminase, aspartate aminotransferase, and gamma-glutamyl transferase in adults. METHODS Two independent researchers systematically searched PubMed, EMBASE, Scopus, Web of Science, and the Cochrane Library for English-language RCTs published up to April 2024. The results were generated through a random-effects model and presented as the weighted mean difference (WMD) with a 95% CI. The Cochrane Risk of Bias Tool for RCTs and Grading of Recommendations Assessment, Development, and Evaluation assessment were used to evaluate quality assessment and certainty of evidence. FINDINGS A total of 21 RCTs were included. A pooled analysis of 24 trials reported that propolis consumption led to a significant reduction in fasting blood glucose (WMD, -9.75 mg/dL; 95% CI, -16.14 to -3.35), insulin (WMD, -1.64 µU/mL; 95% CI, -2.61 to -0.68), glycosylated hemoglobin (WMD, -0.46%; 95% CI, -0.71 to -0.21), homeostatic model assessment of insulin resistance (WMD, -0.54; 95% CI, -0.98 to -0.09), alanine transaminase (WMD, -2.60 IU/L; 95% CI, -4.58 to -0.61), and aspartate aminotransferase (WMD, -2.07 IU/L; 95% CI, -3.05 to -1.09). However, there were no significant effects on gamma-glutamyl transferase in comparison with the control group. IMPLICATIONS This meta-analysis has shown that propolis supplementation may have beneficial effects on glycemic indices and liver enzymes. Future high-quality, long-term RCTs are needed to confirm our results. CLINICALTRIALS gov identifiers: CRD42024524763. (Clin Ther. 2024;46:XXX-XXX) © 2024 Elsevier HS Journals, Inc.
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Affiliation(s)
- Shaghayegh Adeli
- Department of Biochemistry and Diet Therapy, Faculty of Nutrition and Food Sciences, Tabriz University of Medical Sciences, Tabriz, Iran
| | - Mahsa Maroofi
- Department of Clinical Nutrition & Dietetics, Faculty of Nutrition Sciences and Food Technology, Shahid Beheshti University of Medical Sciences, Tehran, Iran
| | | | - Beitullah Alipour
- Department of Community Nutrition, Faculty of Nutrition and Food Science, Tabriz University of Medical Sciences, Tabriz, Iran
| | - Marzieh Heidari
- Department of Biochemistry and Diet Therapy, Faculty of Nutrition and Food Sciences, Tabriz University of Medical Sciences, Tabriz, Iran
| | - Mahdi Vajdi
- Department of Community Nutrition, School of Nutrition and Food Science, Isfahan University of Medical Sciences, Isfahan, Iran.
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19
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Ramamoorthy P, Ramamoorthy S, Santhosh T, samayan K. A Case Report of Auditory and Vestibular Findings in a Patient with Rheumatoid Arthritis and Diabetes Mellitus. Indian J Otolaryngol Head Neck Surg 2024; 76:3656-3660. [PMID: 39130318 PMCID: PMC11306714 DOI: 10.1007/s12070-024-04668-x] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/04/2024] [Accepted: 03/22/2024] [Indexed: 08/13/2024] Open
Abstract
This single case study describes the audiological and vestibular findings of a female patient, aged 62, with diabetes mellitus and rheumatoid arthritis. Based on this case study, we hypothesize that individuals with diabetes mellitus and rheumatoid arthritis are more vulnerable to vestibular impairment. The current findings indicate that central vestibular lesions and bilateral sensorineural hearing loss are related to rheumatoid arthritis and diabetes. Therefore concluding early detection and follow-up is required to understand pathophysiology in detail.
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Affiliation(s)
- Pranesh Ramamoorthy
- Department of Audiology, SRM Institute of Science and Technology, Kattangulathur, Chengalpattu, 603203 India
| | - Santhoshi Ramamoorthy
- Department of Audiology, SRM Institute of Science and Technology, Kattangulathur, Chengalpattu, 603203 India
| | - Tessa Santhosh
- SRM Institute of Science and Technology, Kattangulathur, Chengalpattu, 603203 India
| | - Kala samayan
- SRM Institute of Science and Technology, Kattangulathur, Chengalpattu, 603203 India
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20
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Balci B, Tekce BK, Aktas G. Evaluation of serum oxidative stress levels and antioxidant capacity in prediabetes. ADVANCES IN REDOX RESEARCH 2024; 12:100106. [DOI: 10.1016/j.arres.2024.100106] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 09/25/2024]
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Zhang L, Li Y, Wang H, Guo Y, Wang X, Wu H, Zhang Q, Liu L, Meng G, Zhang S, Sun S, Zhou M, Jia Q, Song K, Stubbendorff A, Gu Y, Niu K. Serum immunoglobulin concentrations and risk of type 2 diabetes mellitus in adults: a prospective cohort study from the TCLSIH study. BMC Immunol 2024; 25:52. [PMID: 39075358 PMCID: PMC11285130 DOI: 10.1186/s12865-024-00637-9] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/29/2023] [Accepted: 06/28/2024] [Indexed: 07/31/2024] Open
Abstract
Type 2 diabetes mellitus (T2DM) is a metabolic disorder characterized by hyperglycemia resulting from defects in insulin secretion and/or insulin action. Increasing evidence suggests that inflammation played an important role in the pathogenesis of T2DM. Prospective studies on the link between immunoglobulins concentrations and the risk of T2DM in adults are limited. We developed a cohort study including 7,093 adults without T2DM history. The incidence of T2DM was 16.45 per 1,000 person-years. Compared with the lowest quartiles, the hazard ratios (95% confidence intervals) of T2DM for the highest quartiles of IgG, IgE, IgM and IgA were 0.64 (0.48-0.85), 0.94 (0.72-1.23), 0.68 (0.50-0.92) and 1.62 (1.24-2.11) (P for trend was < 0.01, 0.84, 0.02 and < 0.0001), respectively, suggesting that serum IgG and IgM concentrations were inversely associated with the incidence of T2DM, and IgA levels were positively associated with the risk of T2DM in a general adult population.
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Affiliation(s)
- Li Zhang
- Tianjin First Center Hospital Health Department, Tianjin, China
| | - Yuanbin Li
- School of Public Health of Tianjin, University of Traditional Chinese Medicine, 10 Poyanghu Road, West Area, Tuanbo New Town, Jinghai District, Tianjin, 301617, China
- School of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China
- Nutritional Epidemiology Institute, School of Public Health, Tianjin Medical University, Tianjin, China
| | - Honglei Wang
- Wuqing District Centers for Disease Control and Prevention, Tianjin, China
| | - Yirui Guo
- Tianjin First Center Hospital Health Department, Tianjin, China
| | - Xiaotong Wang
- Nutritional Epidemiology Institute, School of Public Health, Tianjin Medical University, Tianjin, China
| | - Hongmei Wu
- Nutritional Epidemiology Institute, School of Public Health, Tianjin Medical University, Tianjin, China
| | - Qing Zhang
- Health Management Centre, Tianjin Medical University General Hospital, Tianjin, China
| | - Li Liu
- Health Management Centre, Tianjin Medical University General Hospital, Tianjin, China
| | - Ge Meng
- Nutritional Epidemiology Institute, School of Public Health, Tianjin Medical University, Tianjin, China
| | - Shunming Zhang
- Nutritional Epidemiology Institute, School of Public Health, Tianjin Medical University, Tianjin, China
| | - Shaomei Sun
- Health Management Centre, Tianjin Medical University General Hospital, Tianjin, China
| | - Ming Zhou
- Health Management Centre, Tianjin Medical University General Hospital, Tianjin, China
| | - Qiyu Jia
- Health Management Centre, Tianjin Medical University General Hospital, Tianjin, China
| | - Kun Song
- Health Management Centre, Tianjin Medical University General Hospital, Tianjin, China
| | - Anna Stubbendorff
- Nutritional Epidemiology, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden
| | - Yeqing Gu
- Institute of Radiation Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China.
| | - Kaijun Niu
- School of Public Health of Tianjin, University of Traditional Chinese Medicine, 10 Poyanghu Road, West Area, Tuanbo New Town, Jinghai District, Tianjin, 301617, China.
- School of Integrative Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, China.
- Nutritional Epidemiology Institute, School of Public Health, Tianjin Medical University, Tianjin, China.
- Health Management Centre, Tianjin Medical University General Hospital, Tianjin, China.
- Institute of Radiation Medicine, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China.
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Ibrahim MA, Isah MB, Inim MD, Abdullahi AD, Adamu A. The connections of sialic acids and diabetes mellitus: therapeutic or diagnostic value? Glycobiology 2024; 34:cwae053. [PMID: 39041707 DOI: 10.1093/glycob/cwae053] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/11/2024] [Revised: 06/16/2024] [Accepted: 07/19/2024] [Indexed: 07/24/2024] Open
Abstract
Modulation of sialic acids is one of the important pathological consequences of both type 1 and type 2 diabetes mellitus with or without the micro- and macrovascular complications. However, the mechanistic, therapeutic and/or diagnostic implications of these observations are uncoordinated and possibly conflicting. This review critically analyses the scientific investigations connecting sialic acids with diabetes mellitus. Generally, variations in the levels and patterns of sialylation, fucosylation and galactosylation were predominant across various tissues and body systems of diabetic patients, but the immune system seemed to be most affected. These might be explored as a basis for differential diagnosis of various diabetic complications. Sialic acids are predominantly elevated in nearly all forms of diabetic conditions, particularly nephropathy and retinopathy, which suggests some diagnostic value but the mechanistic details were not unequivocal from the available data. The plausible mechanistic explanations for the elevated sialic acids are increased desialylation by sialidases, stimulation of hexosamine pathway and synthesis of acute phase proteins as well as oxidative stress. Additionally, sialic acids are also profoundly associated with glucose transport and insulin resistance in human-based studies while animal-based studies revealed that the increased desialylation of insulin receptors by sialidases, especially NEU1, might be the causal link. Interestingly, inhibition of the diabetes-associated NEU1 desialylation was beneficial in diabetes management and might be considered as a therapeutic target. It is hoped that the article will provide an informed basis for future research activities on the exploitation of sialic acids and glycobiology for therapeutic and/or diagnostic purposes against diabetes mellitus.
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Affiliation(s)
| | - Murtala Bindawa Isah
- Department of Biochemistry, Umaru Musa Yar'adua University, P.M.B. 2218, Katsina, Nigeria
| | - Mayen David Inim
- Department of Biochemistry, Ahmadu Bello University, Samaru, 80001, Zaria, Nigeria
| | | | - Auwal Adamu
- Department of Biochemistry, Ahmadu Bello University, Samaru, 80001, Zaria, Nigeria
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Guan J, Abudouaini H, Lin K, Yang K. Emerging insights into the role of IL-1 inhibitors and colchicine for inflammation control in type 2 diabetes. Diabetol Metab Syndr 2024; 16:140. [PMID: 38918878 PMCID: PMC11197348 DOI: 10.1186/s13098-024-01369-x] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/26/2024] [Accepted: 05/30/2024] [Indexed: 06/27/2024] Open
Abstract
Type 2 diabetes mellitus (T2DM), a prevalent chronic metabolic disorder, is closely linked to persistent low-grade inflammation, significantly contributing to its development and progression. This review provides a comprehensive examination of the inflammatory mechanisms underlying T2DM, focusing on the role of the NLRP3 inflammasome and interleukin-1β (IL-1β) in mediating inflammatory responses. We discuss the therapeutic potential of IL-1 inhibitors and colchicine, highlighting their mechanisms in inhibiting the NLRP3 inflammasome and reducing IL-1β production. Recent studies indicate that these agents could effectively mitigate inflammation, offering promising avenues for the prevention and management of T2DM. By exploring the intricate connections between metabolic disturbances and chronic inflammation, this review underscores the need for novel anti-inflammatory strategies to address T2DM and its complications.
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Affiliation(s)
- Jianbin Guan
- Honghui-Hospital, Xi'an Jiaotong University, Xi'an, 710054, Shaanxi, China
| | - Haimiti Abudouaini
- Honghui-Hospital, Xi'an Jiaotong University, Xi'an, 710054, Shaanxi, China
| | - Kaiyuan Lin
- Honghui-Hospital, Xi'an Jiaotong University, Xi'an, 710054, Shaanxi, China.
| | - Kaitan Yang
- Honghui-Hospital, Xi'an Jiaotong University, Xi'an, 710054, Shaanxi, China.
- Truma Rehabilitation Department, Honghui-Hospital,Xi'an Jiaotong University, Xi'an, 710054, Shaanxi, China.
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Huang Y, Liu HM, Mao QY, Wu LL, Xiang RL, Yu GY. Identification of circRNAs expression profiles and functional networks in parotid gland of type 2 diabetes mouse. BMC Genomics 2024; 25:450. [PMID: 38714918 PMCID: PMC11077881 DOI: 10.1186/s12864-024-10290-6] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/16/2023] [Accepted: 04/08/2024] [Indexed: 05/12/2024] Open
Abstract
BACKGROUND Circular RNAs (circRNAs) are a novel kind of non-coding RNAs proved to play crucial roles in the development of multiple diabetic complications. However, their expression and function in diabetes mellitus (DM)-impaired salivary glands are unknown. RESULTS By using microarray technology, 663 upregulated and 999 downregulated circRNAs companied with 813 upregulated and 525 downregulated mRNAs were identified in the parotid glands (PGs) of type2 DM mice under a 2-fold change and P < 0.05 cutoff criteria. Gene ontology (GO) and kyoto encyclopedia of genes and genomes (KEGG) analysis of upregulated mRNAs showed enrichments in immune system process and peroxisome proliferator-activated receptor (PPAR) signaling pathway. Infiltration of inflammatory cells and increased inflammatory cytokines were observed in diabetic PGs. Seven differently expressed circRNAs validated by qRT-PCR were selected for coding-non-coding gene co-expression (CNC) and competing endogenous RNA (ceRNA) networks analysis. PPAR signaling pathway was primarily enriched through analysis of circRNA-mRNA networks. Moreover, the circRNA-miRNA-mRNA networks highlighted an enrichment in the regulation of actin cytoskeleton. CONCLUSION The inflammatory response is elevated in diabetic PGs. The selected seven distinct circRNAs may attribute to the injury of diabetic PG by modulating inflammatory response through PPAR signaling pathway and actin cytoskeleton in diabetic PGs.
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Affiliation(s)
- Yan Huang
- Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology & National Center of Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices & Beijing Key Laboratory of Digital Stomatology & Research Center of Engineering and Technology for Computerized Dentistry Ministry of Health & NMPA Key Laboratory for Dental Materials, 100081, Beijing, P.R. China
- Department of Oral and Maxillofacial Surgery, Stomatological Hospital of Xiamen Medical College, Xiamen Key Laboratory of Stomotalogical Disease Diagnosis and Treatment, 361006, Xiamen, P.R. China
| | - Hui-Min Liu
- Department of Physiology and Pathophysiology, Peking University School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, 100191, Beijing, P.R. China
| | - Qian-Ying Mao
- Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology & National Center of Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices & Beijing Key Laboratory of Digital Stomatology & Research Center of Engineering and Technology for Computerized Dentistry Ministry of Health & NMPA Key Laboratory for Dental Materials, 100081, Beijing, P.R. China
| | - Li-Ling Wu
- Department of Physiology and Pathophysiology, Peking University School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, 100191, Beijing, P.R. China
| | - Ruo-Lan Xiang
- Department of Physiology and Pathophysiology, Peking University School of Basic Medical Sciences, State Key Laboratory of Vascular Homeostasis and Remodeling, 100191, Beijing, P.R. China.
| | - Guang-Yan Yu
- Department of Oral and Maxillofacial Surgery, Peking University School and Hospital of Stomatology & National Center of Stomatology & National Clinical Research Center for Oral Diseases & National Engineering Research Center of Oral Biomaterials and Digital Medical Devices & Beijing Key Laboratory of Digital Stomatology & Research Center of Engineering and Technology for Computerized Dentistry Ministry of Health & NMPA Key Laboratory for Dental Materials, 100081, Beijing, P.R. China.
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Yang K, Zeng J, Wu H, Liu H, Ding Z, Liang W, Wu L, Lin Z, Huang W, Xu J, Dong F. Nonalcoholic Fatty Liver Disease: Changes in Gut Microbiota and Blood Lipids. J Clin Transl Hepatol 2024; 12:333-345. [PMID: 38638378 PMCID: PMC11022063 DOI: 10.14218/jcth.2023.00199] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/26/2023] [Revised: 10/10/2023] [Accepted: 11/29/2023] [Indexed: 04/20/2024] Open
Abstract
BACKGROUND AND AIMS The global prevalence of nonalcoholic fatty liver disease (NAFLD) is 25%. This study aimed to explore differences in the gut microbial community and blood lipids between normal livers and those affected by NAFLD using 16S ribosomal deoxyribonucleic acid sequencing. METHODS Gut microbiome profiles of 40 NAFLD and 20 non-NAFLD controls were analyzed. Information about four blood lipids and 13 other clinical features was collected. Patients were divided into three groups by ultrasound and FibroScan, those with a normal liver, mild FL (FL1), and moderate-to-severe FL (FL2). FL1 and FL2 patients were divided into two groups, those with either hyperlipidemia or non-hyperlipidemia based on their blood lipids. Potential keystone species within the groups were identified using univariate analysis and a specificity-occupancy plot. Significant difference in biochemical parameters ion NAFLD patients and healthy individuals were identified by detrended correspondence analysis and canonical correspondence analysis. RESULTS Decreased gut bacterial diversity was found in patients with NAFLD. Firmicutes/Bacteroidetes decreased as NAFLD progressed. Faecalibacterium and Ruminococcus 2 were the most representative fatty-related bacteria. Glutamate pyruvic transaminase, aspartate aminotransferase, and white blood cell count were selected as the most significant biochemical indexes. Calculation of areas under the curve identified two microbiomes combined with the three biochemical indexes that identified normal liver and FL2 very well but performed poorly in diagnosing FL1. CONCLUSIONS Faecalibacterium and Ruminococcus 2, combined with glutamate pyruvic transaminase, aspartate aminotransferase, and white blood cell count distinguished NAFLD. We speculate that regulating the health of gut microbiota may release NAFLD, in addition to providing new targets for clinicians to treat NAFLD.
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Affiliation(s)
| | | | - Huaiyu Wu
- Department of Ultrasound, Shenzhen People’s Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen,Guangdong, China
| | - Huiyu Liu
- Department of Ultrasound, Shenzhen People’s Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen,Guangdong, China
| | - Zhimin Ding
- Department of Ultrasound, Shenzhen People’s Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen,Guangdong, China
| | - Weiyu Liang
- Department of Ultrasound, Shenzhen People’s Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen,Guangdong, China
| | - Linghu Wu
- Department of Ultrasound, Shenzhen People’s Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen,Guangdong, China
| | - Ziwei Lin
- Department of Ultrasound, Shenzhen People’s Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen,Guangdong, China
| | - Wenhui Huang
- Department of Ultrasound, Shenzhen People’s Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen,Guangdong, China
| | - Jinfeng Xu
- Department of Ultrasound, Shenzhen People’s Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen,Guangdong, China
| | - Fajin Dong
- Department of Ultrasound, Shenzhen People’s Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen,Guangdong, China
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Cheng W, Li T, Wang X, Xu T, Zhang Y, Chen J, Wei Z. The neutrophil-to-apolipoprotein A1 ratio is associated with adverse outcomes in patients with acute decompensated heart failure at different glucose metabolic states: a retrospective cohort study. Lipids Health Dis 2024; 23:118. [PMID: 38649986 PMCID: PMC11034163 DOI: 10.1186/s12944-024-02104-1] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/25/2024] [Accepted: 04/06/2024] [Indexed: 04/25/2024] Open
Abstract
BACKGROUND The present study was performed to assess the association between the neutrophil-to-apolipoprotein A1 ratio (NAR) and outcomes in patients with acute decompensated heart failure (ADHF) at different glucose metabolism states. METHODS We recruited 1233 patients with ADHF who were admitted to Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University from December 2014 to October 2019. The endpoints were defined as composites of cardiovascular death, nonfatal myocardial infarction, nonfatal ischemic stroke and exacerbation of chronic heart failure. The restricted cubic spline was used to determine the best cutoff of NAR, and patients were divided into low and high NAR groups. Kaplan-Meier plots and multivariable Cox proportional hazard models were used to investigate the association between NAR and the risk of adverse outcomes. RESULTS During the five-year follow-up period, the composite outcome occurred in 692 participants (56.1%). After adjusting for potential confounding factors, a higher NAR was associated with a higher incidence of composite outcomes in the total cohort (Model 1: HR = 1.42, 95% CI = 1.22-1.65, P<0.001; Model 2: HR = 1.29, 95% CI = 1.10-1.51, P = 0.002; Model 3: HR = 1.20, 95% CI = 1.01-1.42, P = 0.036). At different glucose metabolic states, a high NAR was associated with a high risk of composite outcomes in patients with diabetes mellitus (DM) (Model 1: HR = 1.54, 95% CI = 1.25-1.90, P<0.001; Model 2: HR = 1.40, 95% CI = 1.13-1.74, P = 0.002; Model 3: HR = 1.31, 95% CI = 1.04-1.66, P = 0.022), and the above association was not found in patients with prediabetes mellitus (Pre-DM) or normal glucose regulation (NGR) (both P>0.05). CONCLUSIONS The NAR has predictive value for adverse outcomes of ADHF with DM, which implies that the NAR could be a potential indicator for the management of ADHF.
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Affiliation(s)
- Weimeng Cheng
- Department of Cardiology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210008, China
| | - Tianyue Li
- Department of Cardiology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210008, China
| | - Xiaohan Wang
- Department of Cardiology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210008, China
| | - Tingting Xu
- Department of Cardiology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210008, China
| | - Ying Zhang
- Department of Cardiology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210008, China
| | - Jianzhou Chen
- Department of Cardiology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210008, China.
| | - Zhonghai Wei
- Department of Cardiology, Nanjing Drum Tower Hospital, Affiliated Hospital of Medical School, Nanjing University, Nanjing, 210008, China.
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Jayedi A, Zargar MS, Emadi A, Aune D. Walking speed and the risk of type 2 diabetes: a systematic review and meta-analysis. Br J Sports Med 2024; 58:334-342. [PMID: 38050034 DOI: 10.1136/bjsports-2023-107336] [Citation(s) in RCA: 1] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 10/24/2023] [Indexed: 12/06/2023]
Abstract
OBJECTIVE To investigate the association between walking speed and the risk of type 2 diabetes. DESIGN Systematic review and meta-analysis. DATA SOURCES PubMed, Scopus, CENTRAL and Web of Science to 30 May 2023. ELIGIBILITY CRITERIA FOR SELECTING STUDIES We included cohort studies that explored the association between walking speed and the risk of type 2 diabetes in adults. We used random-effects meta-analyses to calculate relative risk (RR) and risk difference (RD). We rated the credibility of subgroup differences and the certainty of evidence using the Instrument to assess the Credibility of Effect Modification ANalyses (ICEMAN) and Grading of Recommendations Assessment, Development and Evaluation (GRADE) tools, respectively. RESULTS Ten cohort studies were included. Compared with easy/casual walking (<3.2 km/hour), the RR of type 2 diabetes was 0.85 (95% CI 0.70 to 1.00); RD=0.86 (95% CI 1.72 to 0) fewer cases per 100 patients; n=4, GRADE=low) for average/normal walking (3.2-4.8 km/hour), 0.76 (95% CI 0.65 to 0.87); RD=1.38 (95% CI 2.01 to 0.75) fewer cases per 100 patients; n=10, GRADE=low) for fairly brisk walking (4.8-6.4 km/hour) and 0.61 (95% CI 0.49 to 0.73; RD=2.24 (95% CI 2.93 to 1.55) fewer cases per 100 patients; n=6, GRADE=moderate) for brisk/striding walking (>6.4 km/hour). There was no significant or credible difference across subgroups based on adjustment for the total volume of physical activity and time spent walking per day. Dose-response analysis suggested that the risk of type 2 diabetes decreased significantly at a walking speed of 4 km/h and above. CONCLUSIONS Low to moderate certainty evidence, mainly from studies with a high risk of bias, suggests that walking at faster speeds is associated with a graded decrease in the risk of type 2 diabetes. PROSPERO REGISTRATION NUMBER CRD42023432795.
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Affiliation(s)
- Ahmad Jayedi
- Social Determinants of Health Research Center, Semnan University of Medical Sciences, Semnan, Iran
| | - Mahdieh-Sadat Zargar
- Clinical Research Development Unit, Kowsar Educational, Research and Therapeutic Hospital, Semnan University of Medical Sciences, Semnan, Iran
| | - Alireza Emadi
- Food Safety Research Center (salt), Semnan University of Medical Sciences, Semnan, Iran
| | - Dagfinn Aune
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK
- Department of Nutrition, Oslo New University College, Oslo, Norway
- Department of Research, The Cancer Registry of Norway, Oslo, Norway
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Dumont BL, Neagoe PE, Charles E, Villeneuve L, Tardif JC, Räkel A, White M, Sirois MG. Low-Density Neutrophils Contribute to Subclinical Inflammation in Patients with Type 2 Diabetes. Int J Mol Sci 2024; 25:1674. [PMID: 38338951 PMCID: PMC10855851 DOI: 10.3390/ijms25031674] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/09/2024] [Revised: 01/24/2024] [Accepted: 01/25/2024] [Indexed: 02/12/2024] Open
Abstract
Type 2 diabetes (T2D) is characterized by low-grade inflammation. Low-density neutrophils (LDNs) represent normally less than 2% of total neutrophils but increase in multiple pathologies, releasing inflammatory cytokines and neutrophil extracellular traps (NETs). We assessed the count and role of high-density neutrophils (HDNs), LDNs, and NET-related activities in patients with T2D. HDNs and LDNs were purified by fluorescence-activated cell sorting (FACS) and counted by flow cytometry. Circulating inflammatory and NETs biomarkers were measured by ELISA (Enzyme Linked Immunosorbent Assay). NET formation was quantified by confocal microscopy. Neutrophil adhesion onto a human extracellular matrix (hECM) was assessed by optical microscopy. We recruited 22 healthy volunteers (HVs) and 18 patients with T2D. LDN counts in patients with diabetes were significantly higher (160%), along with circulating NETs biomarkers (citrullinated H3 histone (H3Cit), myeloperoxidase (MPO), and MPO-DNA (137%, 175%, and 69%, respectively) versus HV. Circulating interleukins (IL-6 and IL-8) and C-Reactive Protein (CRP) were significantly increased by 117%, 171%, and 79%, respectively, in patients compared to HVs. Isolated LDNs from patients expressed more H3Cit, MPO, and NETs, formed more NETs, and adhered more on hECM compared to LDNs from HVs. Patients with T2D present higher levels of circulating LDN- and NET-related biomarkers and associated pro-inflammatory activities.
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Affiliation(s)
- Benjamin L. Dumont
- Research Center, Montreal Heart Institute, Montreal, QC H1T 1C8, Canada; (B.L.D.); (P.-E.N.); (E.C.); (L.V.); (J.-C.T.)
- Department of Pharmacology and Physiology, Faculty of Medicine, Université de Montréal, Montreal, QC H3C 3J7, Canada
| | - Paul-Eduard Neagoe
- Research Center, Montreal Heart Institute, Montreal, QC H1T 1C8, Canada; (B.L.D.); (P.-E.N.); (E.C.); (L.V.); (J.-C.T.)
| | - Elcha Charles
- Research Center, Montreal Heart Institute, Montreal, QC H1T 1C8, Canada; (B.L.D.); (P.-E.N.); (E.C.); (L.V.); (J.-C.T.)
- Department of Pharmacology and Physiology, Faculty of Medicine, Université de Montréal, Montreal, QC H3C 3J7, Canada
| | - Louis Villeneuve
- Research Center, Montreal Heart Institute, Montreal, QC H1T 1C8, Canada; (B.L.D.); (P.-E.N.); (E.C.); (L.V.); (J.-C.T.)
| | - Jean-Claude Tardif
- Research Center, Montreal Heart Institute, Montreal, QC H1T 1C8, Canada; (B.L.D.); (P.-E.N.); (E.C.); (L.V.); (J.-C.T.)
- Department of Medicine, Faculty of Medicine, Université de Montréal, Montreal, QC H3T 1J4, Canada;
| | - Agnès Räkel
- Department of Medicine, Faculty of Medicine, Université de Montréal, Montreal, QC H3T 1J4, Canada;
- Research Center, Centre Hospitalier de l’Université de Montréal (CHUM), Montreal, QC H2X 0A9, Canada
| | - Michel White
- Research Center, Montreal Heart Institute, Montreal, QC H1T 1C8, Canada; (B.L.D.); (P.-E.N.); (E.C.); (L.V.); (J.-C.T.)
- Department of Medicine, Faculty of Medicine, Université de Montréal, Montreal, QC H3T 1J4, Canada;
| | - Martin G. Sirois
- Research Center, Montreal Heart Institute, Montreal, QC H1T 1C8, Canada; (B.L.D.); (P.-E.N.); (E.C.); (L.V.); (J.-C.T.)
- Department of Pharmacology and Physiology, Faculty of Medicine, Université de Montréal, Montreal, QC H3C 3J7, Canada
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Qiang YX, You J, He XY, Guo Y, Deng YT, Gao PY, Wu XR, Feng JF, Cheng W, Yu JT. Plasma metabolic profiles predict future dementia and dementia subtypes: a prospective analysis of 274,160 participants. Alzheimers Res Ther 2024; 16:16. [PMID: 38254212 PMCID: PMC10802055 DOI: 10.1186/s13195-023-01379-3] [Citation(s) in RCA: 18] [Impact Index Per Article: 18.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/19/2023] [Accepted: 12/30/2023] [Indexed: 01/24/2024]
Abstract
BACKGROUND Blood-based biomarkers for dementia are gaining attention due to their non-invasive nature and feasibility in regular healthcare settings. Here, we explored the associations between 249 metabolites with all-cause dementia (ACD), Alzheimer's disease (AD), and vascular dementia (VaD) and assessed their predictive potential. METHODS This study included 274,160 participants from the UK Biobank. Cox proportional hazard models were employed to investigate longitudinal associations between metabolites and dementia. The importance of these metabolites was quantified using machine learning algorithms, and a metabolic risk score (MetRS) was subsequently developed for each dementia type. We further investigated how MetRS stratified the risk of dementia onset and assessed its predictive performance, both alone and in combination with demographic and cognitive predictors. RESULTS During a median follow-up of 14.01 years, 5274 participants developed dementia. Of the 249 metabolites examined, 143 were significantly associated with incident ACD, 130 with AD, and 140 with VaD. Among metabolites significantly associated with dementia, lipoprotein lipid concentrations, linoleic acid, sphingomyelin, glucose, and branched-chain amino acids ranked top in importance. Individuals within the top tertile of MetRS faced a significantly greater risk of developing dementia than those in the lowest tertile. When MetRS was combined with demographic and cognitive predictors, the model yielded the area under the receiver operating characteristic curve (AUC) values of 0.857 for ACD, 0.861 for AD, and 0.873 for VaD. CONCLUSIONS We conducted the largest metabolome investigation of dementia to date, for the first time revealed the metabolite importance ranking, and highlighted the contribution of plasma metabolites for dementia prediction.
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Affiliation(s)
- Yi-Xuan Qiang
- Department of Neurology and National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Huashan Hospital, Shanghai Medical College, Fudan University, 12Th Wulumuqi Zhong Road, Shanghai, 200040, China
| | - Jia You
- Department of Neurology and National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Huashan Hospital, Shanghai Medical College, Fudan University, 12Th Wulumuqi Zhong Road, Shanghai, 200040, China
- Institute of Science and Technology for Brain-Inspired Intelligence, Fudan University, Shanghai, 200433, China
| | - Xiao-Yu He
- Department of Neurology and National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Huashan Hospital, Shanghai Medical College, Fudan University, 12Th Wulumuqi Zhong Road, Shanghai, 200040, China
| | - Yu Guo
- Department of Neurology and National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Huashan Hospital, Shanghai Medical College, Fudan University, 12Th Wulumuqi Zhong Road, Shanghai, 200040, China
| | - Yue-Ting Deng
- Department of Neurology and National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Huashan Hospital, Shanghai Medical College, Fudan University, 12Th Wulumuqi Zhong Road, Shanghai, 200040, China
| | - Pei-Yang Gao
- Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, 266011, China
| | - Xin-Rui Wu
- Department of Neurology and National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Huashan Hospital, Shanghai Medical College, Fudan University, 12Th Wulumuqi Zhong Road, Shanghai, 200040, China
| | - Jian-Feng Feng
- Institute of Science and Technology for Brain-Inspired Intelligence, Fudan University, Shanghai, 200433, China
- Key Laboratory of Computational Neuroscience and Brain-Inspired Intelligence, Ministry of Education, Fudan University, Shanghai, 200433, China
- Department of Computer Science, University of Warwick, Coventry, CV4 7AL, UK
| | - Wei Cheng
- Department of Neurology and National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Huashan Hospital, Shanghai Medical College, Fudan University, 12Th Wulumuqi Zhong Road, Shanghai, 200040, China.
- Institute of Science and Technology for Brain-Inspired Intelligence, Fudan University, Shanghai, 200433, China.
- Key Laboratory of Computational Neuroscience and Brain-Inspired Intelligence, Ministry of Education, Fudan University, Shanghai, 200433, China.
- Department of Computer Science, University of Warwick, Coventry, CV4 7AL, UK.
| | - Jin-Tai Yu
- Department of Neurology and National Center for Neurological Disorders, State Key Laboratory of Medical Neurobiology and MOE Frontiers Center for Brain Science, Huashan Hospital, Shanghai Medical College, Fudan University, 12Th Wulumuqi Zhong Road, Shanghai, 200040, China.
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Hasan I, Rainsford KD, Ross JS. Salsalate: a pleotropic anti-inflammatory drug in the treatment of diabetes, obesity, and metabolic diseases. Inflammopharmacology 2023; 31:2781-2797. [PMID: 37758933 DOI: 10.1007/s10787-023-01242-9] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/17/2023] [Accepted: 04/12/2023] [Indexed: 09/29/2023]
Abstract
Type two Diabetes Mellitus (T2DM) is a rising epidemic. Available therapeutic strategies have provided glycaemic control via HbA1c reduction but fail to provide clinically meaningful reduction in microvascular and macrovascular (cardiac, renal, ophthalmological, and neurological) complications. Inflammation is strongly linked to the pathogenesis of T2DM. Underlying inflammatory mechanisms include oxidative stress, endoplasmic reticulum stress amyloid deposition in the pancreas, lipotoxicity, and glucotoxicity. Molecular signalling mechanisms in chronic inflammation linked to obesity and diabetes include JANK, NF-kB, and AMPK pathways. These activated pathways lead to a production of various inflammatory cytokines, such as Interleukin (IL-6), tumor necrosis factor (TNF)-alpha, and C-reactive protein (CRP), which create a chronic low-grade inflammation and ultimately dysregulation of glucose homeostasis in the liver, skeletal muscle, and smooth muscle. Anti-inflammatory agents are being tested as anti-diabetic agents such as the IL-1b antagonist, Anakinra, the IL-1b inhibitor, Canakinuma, the IL-6 antagonists such as Tocilizumab, Rapamycin (Everolimus), and the IKK-beta kinase inhibitor, Salsalate. Salsalate is a century old safe anti-inflammatory drug used in the treatment of arthritis. Long-term safety and efficacy of Salsalate in the treatment of T2DM have been evaluated, which showed improved fasting plasma glucose and reduced HbA1C levels as well as reduced pro-inflammatory markers in T2DM patients. Current publication summarizes the literature review of pathophysiology of role of inflammation in T2DM and clinical efficacy and safety of Salsalate in the treatment of T2DM.
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Affiliation(s)
- I Hasan
- RH Nanopharmaceuticals LLC, 140 Ocean Ave, Monmouth Beach, New Jersey, 07750, USA.
| | - K D Rainsford
- Emeritus Professor of Biomedical Sciences, Department of Biosciences and Chemistry, BMRC, Sheffield Hallam University, Howard Street, Sheffield, S1 1WB, UK
| | - Joel S Ross
- RH Nanopharmaceuticals LLC, 140 Ocean Ave, Monmouth Beach, New Jersey, 07750, USA
- J & D Pharmaceuticals LLC, Monmouth County, USA
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31
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Shen M, Li Z, Li H, Yan X, Feng B, Xu L. Association of periodontitis and tooth loss with extent of coronary atherosclerosis in patients with type 2 diabetes mellitus. Front Endocrinol (Lausanne) 2023; 14:1243992. [PMID: 38075042 PMCID: PMC10702216 DOI: 10.3389/fendo.2023.1243992] [Citation(s) in RCA: 6] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/21/2023] [Accepted: 11/06/2023] [Indexed: 12/18/2023] Open
Abstract
Aim The objective was to investigate the association of periodontitis and tooth loss with extent of diabetic coronary atherosclerosis. Materials and methods 272 patients who were hospitalized at Shanghai East hospital and underwent a coronary artery calcium (CAC) CT scan were enrolled in this study. Individuals were grouped based on their CAC scores into a normal-to-mild coronary atherosclerosis (AS) group (0 ≤ score ≤ 100, n=184) and a moderate-to-severe group (score≥101, n=88). Periodontitis parameters and number of missing teeth were evaluated for every patient. The severity of periodontitis was categorized as mild, moderate, or severe. The taxonomic composition of the microbiota was determined using full-length 16S ribosomal RNA gene sequencing. Salivary inflammatory factors were tested by ELISA. Results Clinical attachment loss (CAL) (P =0.05) and the number of teeth lost (P = 0.016) were significantly higher in the moderate-to-severe coronary AS group, with these differences being more obvious in younger patients and patients with short-duration diabetes. Multivariate logistic regression analysis revealed that CAL (OR = 1.231, 95% CI = 1.066-1.214, P = 0.047) and having 10-19 missing teeth (OR = 1.604, 95% CI = 1.393-6.555, P = 0.05) were strongly associated with the presence of moderate-to-severe coronary AS. Salivary IL-6 and TNF-α levels, as well as levels of Porphyromonas gingivalis and Neisseria mucosa, were significantly elevated in the moderate-to-severe coronary AS group. Conclusion It was found that both tooth loss and CAL were related to the extent of diabetic coronary AS. Saliva inflammatory factors and oral bacteremia may be new biomarkers for moderate-to-severe coronary AS.
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Affiliation(s)
- Minhua Shen
- Department of Stomatology, East Hospital, Tongji University School of Medicine, Shanghai, China
| | - Zhen Li
- Department of Stomatology, East Hospital, Tongji University School of Medicine, Shanghai, China
| | - Huizhi Li
- Department of Endocrinology, East Hospital, Tongji University School of Medicine, Shanghai, China
| | - Xinfeng Yan
- Department of Endocrinology, East Hospital, Tongji University School of Medicine, Shanghai, China
| | - Bo Feng
- Department of Endocrinology, East Hospital, Tongji University School of Medicine, Shanghai, China
| | - Lei Xu
- Department of Endocrinology, East Hospital, Tongji University School of Medicine, Shanghai, China
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Park MN. Therapeutic Strategies for Pancreatic-Cancer-Related Type 2 Diabetes Centered around Natural Products. Int J Mol Sci 2023; 24:15906. [PMID: 37958889 PMCID: PMC10648679 DOI: 10.3390/ijms242115906] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/25/2023] [Revised: 10/23/2023] [Accepted: 10/30/2023] [Indexed: 11/15/2023] Open
Abstract
Pancreatic ductal adenocarcinoma (PDAC), a highly malignant neoplasm, is classified as one of the most severe and devastating types of cancer. PDAC is a notable malignancy that exhibits a discouraging prognosis and a rising occurrence. The interplay between diabetes and pancreatic cancer exhibits a reciprocal causation. The identified metabolic disorder has been observed to possess noteworthy consequences on health outcomes, resulting in elevated rates of morbidity. The principal mechanisms involve the suppression of the immune system, the activation of pancreatic stellate cells (PSCs), and the onset of systemic metabolic disease caused by dysfunction of the islets. From this point forward, it is important to recognize that pancreatic-cancer-related diabetes (PCRD) has the ability to increase the likelihood of developing pancreatic cancer. This highlights the complex relationship that exists between these two physiological states. Therefore, we investigated into the complex domain of PSCs, elucidating their intricate signaling pathways and the profound influence of chemokines on their behavior and final outcome. In order to surmount the obstacle of drug resistance and eliminate PDAC, researchers have undertaken extensive efforts to explore and cultivate novel natural compounds of the next generation. Additional investigation is necessary in order to comprehensively comprehend the effect of PCRD-mediated apoptosis on the progression and onset of PDAC through the utilization of natural compounds. This study aims to examine the potential anticancer properties of natural compounds in individuals with diabetes who are undergoing chemotherapy, targeted therapy, or immunotherapy. It is anticipated that these compounds will exhibit increased potency and possess enhanced pharmacological benefits. According to our research findings, it is indicated that naturally derived chemical compounds hold potential in the development of PDAC therapies that are both safe and efficacious.
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Affiliation(s)
- Moon Nyeo Park
- Department of Pathology, College of Korean Medicine, Kyung Hee University, Hoegidong Dongdaemungu, Seoul 05253, Republic of Korea
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Wu Y, Chen M, Liu T, Zhou J, Wang Y, Yu L, Zhang J, Tian K. Association between depression and risk of type 2 diabetes and its sociodemographic factors modifications: A prospective cohort study in southwest China. J Diabetes 2023; 15:994-1004. [PMID: 37581248 PMCID: PMC10667669 DOI: 10.1111/1753-0407.13453] [Citation(s) in RCA: 3] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 02/02/2023] [Revised: 06/12/2023] [Accepted: 07/23/2023] [Indexed: 08/16/2023] Open
Abstract
BACKGROUND Depression may be associated with the risk of developing type 2 diabetes. The goal of this study was to explore the association of severe of depression with the risk of type 2 diabetes in adults in Guizhou, China. METHODS A 10-year prospective cohort study of 7158 nondiabetes adults aged 18 years or older was conducted in Guizhou, southwest China from 2010 to 2020. The Patient Health Questionnaire-9 (PHQ-9) was used to measure the prevalence of depression. Cox proportional hazard models were used to estimated hazard ratios (HRs) and 95% confidence intervals (95% CIs) of depression and incident type 2 diabetes. A quantile regression (QR) analytical approach were applied to evaluate the associations of PHQ-9 score with plasma glucose values. RESULTS A total of 739 type 2 diabetes cases were identified during a median follow-up of 6.59 years. The HR (95% CI) per 1-SD increase for baseline PHQ-9 score was 1.051 (1.021, 1.082) after multivariable adjustment. Compared with participants without depression, those with mild or more advanced depression had a higher risk of incident type 2 diabetes (HR:1.440 [95% CI, 1.095, 1.894]). Associations between depression with type 2 diabetes were suggested to be even stronger among women or participants aged ≥45 years (p < .05). There are significant positive associations of PHQ-9 score with 2-h oral glucose tolerance test blood glucose levels. CONCLUSION Depression significantly increased the risk of incident type 2 diabetes, especially in women, participants aged ≥45 years, Han ethnicity, and urban residents. These findings highlighted the importance and urgency of depression health care.
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Affiliation(s)
- Yanli Wu
- Guizhou Center for Disease Control and PreventionGuiyangChina
| | - Min Chen
- Guizhou Center for Disease Control and PreventionGuiyangChina
| | - Tao Liu
- Guizhou Center for Disease Control and PreventionGuiyangChina
| | - Jie Zhou
- Guizhou Center for Disease Control and PreventionGuiyangChina
| | - Yiying Wang
- Guizhou Center for Disease Control and PreventionGuiyangChina
| | - Lisha Yu
- Guizhou Center for Disease Control and PreventionGuiyangChina
| | - Ji Zhang
- Guizhou Center for Disease Control and PreventionGuiyangChina
| | - Kunming Tian
- Department of Preventive Medicine, School of Public HealthZunyi Medical UniversityZunyiChina
- Department of Geriatric Nursing, School of NursingZunyi Medical UniversityZunyiChina
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Fung E, Chan EYS, Ng KH, Yu KM, Li H, Wang Y. Towards clinical application of GlycA and GlycB for early detection of inflammation associated with (pre)diabetes and cardiovascular disease: recent evidence and updates. J Inflamm (Lond) 2023; 20:32. [PMID: 37814278 PMCID: PMC10563214 DOI: 10.1186/s12950-023-00358-7] [Citation(s) in RCA: 4] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/03/2023] [Accepted: 09/18/2023] [Indexed: 10/11/2023] Open
Abstract
Cardiometabolic diseases are associated with low-grade inflammation early in life and persists into old age. The long latency period presents opportunities for early detection, lifestyle modification and intervention. However, the performance of conventional biomarker assays to detect low-grade inflammation has been variable, particularly for early-stage cardiometabolic disorder including prediabetes and subclinical atherosclerotic vascular inflammation. During the last decade, the application of nuclear magnetic resonance (NMR) spectroscopy for metabolic profiling of biofluids in translational and epidemiological research has advanced to a stage approaching clinical application. Proton (1H)-NMR profiling induces no destructible physical changes to specimens, and generates quantitative signals from deconvoluted spectra that are highly repeatable and reproducible. Apart from quantitative analysis of amino acids, lipids/lipoproteins, metabolic intermediates and small proteins, 1H-NMR technology is unique in being able to detect composite signals of acute-phase and low-grade inflammation indicated by glycosylated acetyls (GlycA) and N-acetylneuraminic acid (sialic acid) moieties (GlycB). Different from conventional immunoassays that target epitopes and are susceptible to conformational variation in protein structure and binding, GlycA and GlycB signals are stable over time, and maybe complementary as well as superior to high-sensitivity C-reactive protein and other inflammatory cytokines. Here we review the physicochemical principles behind 1H-NMR profiling of GlycA and GlycB, and the available evidence supporting their potential clinical application for the prediction of incident (pre)diabetes, cardiovascular disease, and adverse outcomes.
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Affiliation(s)
- Erik Fung
- Department of Medicine & Therapeutics, Laboratory for Heart Failure + Circulation Research, Li Ka Shing Institute of Health Sciences, and Centre for Cardiovascular Genomics & Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong SAR, China.
- Hong Kong Hub of Paediatric Excellence, The Chinese University of Hong Kong, Hong Kong Children's Hospital, Kowloon Bay, Kowloon, Hong Kong SAR, China.
- Neural, Vascular, and Metabolic Biology Programme, and Ministry of Education Laboratory for Regenerative Medicine, School of Biomedical Sciences, Faculty of Medicine, Lo Kwee-Seong Integrated Biomedical Sciences Building, Area 39, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong SAR, China.
- Department of Epidemiology & Biostatistics, School of Public Health, St Mary's Campus, Imperial College London, London, UK.
- School of Medicine, The Chinese University of Hong Kong, Shenzhen, China.
- Prince of Wales Hospital, Room 124010, 10/F, LCWCSB, 30-32 Ngan Shing Street, Shatin, New Territories, Hong Kong SAR, China.
| | - Eunice Y S Chan
- School of Medicine, The Chinese University of Hong Kong, Shenzhen, China
| | - Kwan Hung Ng
- Department of Medicine & Therapeutics, Laboratory for Heart Failure + Circulation Research, Li Ka Shing Institute of Health Sciences, and Centre for Cardiovascular Genomics & Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong SAR, China
- Hong Kong Hub of Paediatric Excellence, The Chinese University of Hong Kong, Hong Kong Children's Hospital, Kowloon Bay, Kowloon, Hong Kong SAR, China
| | - Ka Man Yu
- Department of Medicine & Therapeutics, Laboratory for Heart Failure + Circulation Research, Li Ka Shing Institute of Health Sciences, and Centre for Cardiovascular Genomics & Medicine, Faculty of Medicine, The Chinese University of Hong Kong, Shatin, New Territories, Hong Kong SAR, China
- Hong Kong Hub of Paediatric Excellence, The Chinese University of Hong Kong, Hong Kong Children's Hospital, Kowloon Bay, Kowloon, Hong Kong SAR, China
| | - Huijun Li
- School of Medicine, The Chinese University of Hong Kong, Shenzhen, China
| | - Yulan Wang
- Singapore Phenome Centre, Lee Kong Chian School of Medicine, Nanyang Technological University, Singapore, Singapore
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35
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S. Jarab A, Al-Qerem WA, Hamam H, Abu Heshmeh S, Al-Azzam S, L. Mukattash T, Alefishat EA. Glycemic control and its associated factors among diabetic heart failure outpatients at two major hospitals in Jordan. PLoS One 2023; 18:e0285142. [PMID: 37796848 PMCID: PMC10553218 DOI: 10.1371/journal.pone.0285142] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/30/2023] [Accepted: 04/14/2023] [Indexed: 10/07/2023] Open
Abstract
Patients with heart failure (HF) are generally at higher risk of developing type 2 diabetes and having uncontrolled blood glucose. Furthermore, the prevalence of uncontrolled blood glucose in patients with HF is largely unknown. Identifying the factors associated with poor blood glucose control is a preliminary step in the development of effective intervention programs. The current cross-sectional study was conducted at two major hospitals to explore the factors associated with blood glucose control among patients with heart failure and type 2 diabetes. In addition to sociodemographic, medical records were used to collect medical information and a validated questionnaire was used to evaluate medication adherence. Regression analysis showed that poor medication adherence (OR = 0.432; 95%CI 0.204-0.912; P<0.05) and increased white blood cells count (OR = 1.12; 95%CI 1.033-1.213; P<0.01) were associated with poor glycemic control. For enhancing blood glucose control among patients with HF and diabetes, future intervention programs should specifically target patients who have high WBC counts and poor medication.
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Affiliation(s)
- Anan S. Jarab
- Department of Clinical Pharmacy, Faculty of Pharmacy, Jordan University of Science and Technology, Irbid, Jordan
- College of Pharmacy, Al Ain University, Abu Dhabi, United Arab Emirates
| | - Walid A. Al-Qerem
- Department of Pharmacy, Faculty of Pharmacy, Al-Zaytoonah University of Jordan, Amman, Jordan
| | - Hanan Hamam
- Department of Clinical Pharmacy, Faculty of Pharmacy, Jordan University of Science and Technology, Irbid, Jordan
| | - Shrouq Abu Heshmeh
- Department of Clinical Pharmacy, Faculty of Pharmacy, Jordan University of Science and Technology, Irbid, Jordan
| | - Sayer Al-Azzam
- Department of Clinical Pharmacy, Faculty of Pharmacy, Jordan University of Science and Technology, Irbid, Jordan
| | - Tareq L. Mukattash
- Department of Clinical Pharmacy, Faculty of Pharmacy, Jordan University of Science and Technology, Irbid, Jordan
| | - Eman A. Alefishat
- Department of Pharmacology, College of Medicine and Health Science, Khalifa University of Science and Technology, Abu Dhabi, United Arab Emirates
- Department Biopharmaceutics and Clinical Pharmacy, Faculty of Pharmacy, University of Jordan, Amman, Jordan
- Center for Biotechnology, Khalifa University of Science and Technology, Abu Dhabi, United Arab Emirates
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36
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Zhou P, Hao Z, Xu W, Yu J. Effects of Niaoduqing granules on inflammatory response of diabetic kidney disease: A meta‑analysis. Exp Ther Med 2023; 26:494. [PMID: 37745039 PMCID: PMC10515115 DOI: 10.3892/etm.2023.12193] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/18/2022] [Accepted: 07/20/2023] [Indexed: 09/26/2023] Open
Abstract
Diabetic kidney disease (DKD) is one of the most severe chronic microvascular complications of diabetes and the leading cause of end-stage kidney disease worldwide. The mechanism of inflammation underlying DKD has been attracting attention over recent years, but effective therapeutic strategies have remained elusive. Niaoduqing (NDQ) granules are one of the most commonly used drugs for the treatment of DKD in China, and it has therapeutic effects against inflammation in DKD. Therefore, the aim of the present analysis was to evaluate the inflammatory response outcomes and safety of NDQ granules for the treatment of DKD. The following databases were searched from their inception to 31st of May 2023 to obtain published accounts of relevant randomized controlled trials: China National Knowledge Infrastructure, China Science and Technology Journal, Wanfang, The Chinese Biomedicine, PubMed, Web of Science and Cochrane Library. The 'risk of bias' evaluation tool produced by the Cochrane Collaboration Handbook was used for evaluating the quality, whereas Revman software (version 5.3) was used for meta-analysis. In total, 16 studies were included into the present study according to criteria, with a total of 1,526 patients. Compared with those in the control group, the results of the meta-analysis revealed that the combination of conventional treatment and NDQ granules may further decrease C-reactive protein [standardized mean difference (SMD), -1.33; 95% confidence interval (CI), -1.76, -0.91; P<0.00001], TNF-α (SMD, -1.90; 95% CI, -2.35,-1.45; P<0.00001) and IL-6 (SMD, -1.72; 95% CI, -2.52,-0.91; P<0.0001) levels, whilst increasing the clinical effective rate (risk ratio, 1.22; 95% CI, 1.14,1.29; P<0.00001), in patients with DKD. In terms of safety, a total of 34 and 39 patients included in the intervention and in the control group, respectively, developed adverse reactions. Results from the present analysis suggest that NDQ granules may be beneficial in suppressing inflammation caused by DKD when used in combination with conventional treatment, potentially guiding future directions in clinical practice. However, further high-quality studies are needed to confirm the anti-inflammation response in the future.
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Affiliation(s)
- Peipei Zhou
- Department of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210000, P.R. China
- The First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210000, P.R. China
| | - Zhenning Hao
- Department of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210000, P.R. China
- The First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210000, P.R. China
| | - Weilong Xu
- Department of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210000, P.R. China
- The First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210000, P.R. China
| | - Jiangyi Yu
- Department of Endocrinology, Jiangsu Province Hospital of Chinese Medicine, Affiliated Hospital of Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210000, P.R. China
- The First Clinical Medical College, Nanjing University of Chinese Medicine, Nanjing, Jiangsu 210000, P.R. China
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37
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Biavaschi M, Melchiors Morsch VM, Jacobi LF, Hoppen A, Bianchin N, Chitolina Schetinger MR. Predisposition to Type 2 Diabetes in Aspects of the Glycemic Curve and Glycated Hemoglobin in Healthy, Young Adults: A Cross-sectional Study. Can J Diabetes 2023; 47:587-593. [PMID: 37225120 DOI: 10.1016/j.jcjd.2023.05.009] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/10/2023] [Revised: 05/10/2023] [Accepted: 05/16/2023] [Indexed: 05/26/2023]
Abstract
OBJECTIVES Our aim in this study was to identify predictors for diabetes among the characteristics of the glycemic curve and glycated hemoglobin (A1C) in healthy, young adults. METHODS We used a cross-sectional study to establish predictors for diabetes based on earlier studies and evaluated occurrence of the condition in 81 healthy, young adult subjects. These volunteers underwent analysis of fasting plasma glucose, oral glucose tolerance test plasma glucose, A1C, and inflammatory markers (leukocytes, monocytes, and C-reactive protein). The nonparametric Mann-Whitney U test, Fisher's exact test, chi-square test, Kruskal-Wallis test, and multiple-comparisons test were used to analyze the data. RESULTS We studied 2 age groups, homogeneous in terms of family history of diabetes: one group ranged in age from ≥18 to <28 years (median 20 years; body mass index [BMI] 24 kg/m2) and the other group ranged in age from ≥28 to <45 years (median 35 years; BMI 24 kg/m2). The older group had a higher incidence of predictors (p=0.0005) and was associated with the predictors 30-minute blood glucose ≥164 mg/dL (p=0.0190), 60-minute blood glucose ≥125 mg/dL (p=0.0346), and A1C ≥5.5% (p=0.0162), with a monophasic glycemic curve (p=0.007). The younger group was associated with the 2-hour plasma glucose predictor ≥140 mg/dL (p=0.014). All subjects had fasting glucose in the normal range. CONCLUSIONS Healthy, young adults may already have predictors of diabetes, identified mainly by aspects of the glycemic curve and A1C, but at more modest levels than those with prediabetes.
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Affiliation(s)
- Marcelo Biavaschi
- Department of Medical Clinic and Endocrinology, Federal University of Santa Maria, Rio Grande do Sul, Brazil.
| | - Vera Maria Melchiors Morsch
- Department of Biochemistry and Molecular Biology, Postgraduate Program in Biological Sciences: Toxicological Biochemistry, Federal University of Santa Maria, Rio Grande do Sul, Brazil
| | | | - Andressa Hoppen
- Faculty of Medicine, Federal University of Santa Maria, Rio Grande do Sul, Brazil
| | - Nathieli Bianchin
- Department of Biochemistry and Molecular Biology, Postgraduate Program in Biological Sciences: Toxicological Biochemistry, Federal University of Santa Maria, Rio Grande do Sul, Brazil
| | - Maria Rosa Chitolina Schetinger
- Department of Biochemistry and Molecular Biology, Postgraduate Program in Biological Sciences: Toxicological Biochemistry, Federal University of Santa Maria, Rio Grande do Sul, Brazil
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38
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Surachman A, Tucker-Seeley R, Almeida DM. The association between material-psychological-behavioral framework of financial hardship and markers of inflammation: a cross-sectional study of the Midlife in the United States (MIDUS) Refresher cohort. BMC Public Health 2023; 23:1845. [PMID: 37735377 PMCID: PMC10514981 DOI: 10.1186/s12889-023-16745-x] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/21/2022] [Accepted: 09/12/2023] [Indexed: 09/23/2023] Open
Abstract
BACKGROUND Measures of financial hardship have been suggested to supplement traditional indicators of socioeconomic status (SES) to elucidate household economic well-being. This study formally tested the construct validity of financial hardship and examined its association with markers of inflammation. METHODS This study utilized data from the Midlife Development in the United States Refresher Study (MIDUS-R; Age = 23-76, 53.7% female, 71% white). Participants were divided into exploratory factor analysis (EFA; completed SAQs only; N = 2,243) and confirmatory factor analysis sample (CFA; completed SAQs and biomarker assessment; N = 863). Analysis was divided into three steps. First, exploratory factor analysis (EFA) is used to examine if the three-domain factor (material, psychological, and behavioral) is the best fitting model for financial hardship measures. Second, we conducted CFA to test the hypothesized three-factor measurement model of financial hardship. Third, we tested the association between domains and the general latent factor of financial hardship and inflammation (interleukin 6/IL6, c-reactive protein/CRP, and fibrinogen). RESULTS Results from EFA supported the three-domain model of financial hardship. The hypothesized three-domain measurement model fits well in a different sample within MIDUS-R. In the models adjusted for age and sex, higher material hardship was associated with elevated IL6, CRP, and fibrinogen, while higher behavioral hardship was associated with higher CRP. The association between the material domain and IL6 remained significant after adding body mass index, education, and race as additional covariates. The second-order financial hardship measurement model was associated with IL6, CRP, and fibrinogen, adjusted for age, sex, BMI, education, and race. CONCLUSION Explicating the socioeconomic environment to include indicators of financial hardship can help researchers better understand the pathway between SES and the inflammation process, which may help elucidate pathways between SES and age-related chronic diseases associated with inflammation.
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Affiliation(s)
- Agus Surachman
- Department of Epidemiology and Biostatistics, Dornsife School of Public Health, Drexel University, Philadelphia, 19104, USA.
- College of Nursing and Health Professions, Drexel University, Philadelphia, 19104, USA.
| | | | - David M Almeida
- Department of Human Development and Family Studies, The Pennsylvania State University, University Park, PA, 16802, USA
- Center for Healthy Aging, The Pennsylvania State University, University Park, PA, 16802, USA
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39
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Lagou V, Jiang L, Ulrich A, Zudina L, González KSG, Balkhiyarova Z, Faggian A, Maina JG, Chen S, Todorov PV, Sharapov S, David A, Marullo L, Mägi R, Rujan RM, Ahlqvist E, Thorleifsson G, Gao Η, Εvangelou Ε, Benyamin B, Scott RA, Isaacs A, Zhao JH, Willems SM, Johnson T, Gieger C, Grallert H, Meisinger C, Müller-Nurasyid M, Strawbridge RJ, Goel A, Rybin D, Albrecht E, Jackson AU, Stringham HM, Corrêa IR, Farber-Eger E, Steinthorsdottir V, Uitterlinden AG, Munroe PB, Brown MJ, Schmidberger J, Holmen O, Thorand B, Hveem K, Wilsgaard T, Mohlke KL, Wang Z, Shmeliov A, den Hoed M, Loos RJF, Kratzer W, Haenle M, Koenig W, Boehm BO, Tan TM, Tomas A, Salem V, Barroso I, Tuomilehto J, Boehnke M, Florez JC, Hamsten A, Watkins H, Njølstad I, Wichmann HE, Caulfield MJ, Khaw KT, van Duijn CM, Hofman A, Wareham NJ, Langenberg C, Whitfield JB, Martin NG, Montgomery G, Scapoli C, Tzoulaki I, Elliott P, Thorsteinsdottir U, Stefansson K, Brittain EL, McCarthy MI, Froguel P, Sexton PM, Wootten D, Groop L, Dupuis J, Meigs JB, Deganutti G, Demirkan A, Pers TH, Reynolds CA, Aulchenko YS, Kaakinen MA, Jones B, Prokopenko I. GWAS of random glucose in 476,326 individuals provide insights into diabetes pathophysiology, complications and treatment stratification. Nat Genet 2023; 55:1448-1461. [PMID: 37679419 PMCID: PMC10484788 DOI: 10.1038/s41588-023-01462-3] [Citation(s) in RCA: 16] [Impact Index Per Article: 8.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 09/18/2021] [Accepted: 06/27/2023] [Indexed: 09/09/2023]
Abstract
Conventional measurements of fasting and postprandial blood glucose levels investigated in genome-wide association studies (GWAS) cannot capture the effects of DNA variability on 'around the clock' glucoregulatory processes. Here we show that GWAS meta-analysis of glucose measurements under nonstandardized conditions (random glucose (RG)) in 476,326 individuals of diverse ancestries and without diabetes enables locus discovery and innovative pathophysiological observations. We discovered 120 RG loci represented by 150 distinct signals, including 13 with sex-dimorphic effects, two cross-ancestry and seven rare frequency signals. Of these, 44 loci are new for glycemic traits. Regulatory, glycosylation and metagenomic annotations highlight ileum and colon tissues, indicating an underappreciated role of the gastrointestinal tract in controlling blood glucose. Functional follow-up and molecular dynamics simulations of lower frequency coding variants in glucagon-like peptide-1 receptor (GLP1R), a type 2 diabetes treatment target, reveal that optimal selection of GLP-1R agonist therapy will benefit from tailored genetic stratification. We also provide evidence from Mendelian randomization that lung function is modulated by blood glucose and that pulmonary dysfunction is a diabetes complication. Our investigation yields new insights into the biology of glucose regulation, diabetes complications and pathways for treatment stratification.
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Affiliation(s)
- Vasiliki Lagou
- Wellcome Centre for Human Genetics, University of Oxford, Oxford, UK
- Human Genetics, Wellcome Sanger Institute, Hinxton, UK
- VIB-KU Leuven Center for Brain and Disease Research, Leuven, Belgium
| | - Longda Jiang
- Institute for Molecular Bioscience, The University of Queensland, Brisbane, Queensland, Australia
- Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK
| | - Anna Ulrich
- Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK
- Department of Clinical and Experimental Medicine, School of Biosciences and Medicine, University of Surrey, Guildford, UK
| | - Liudmila Zudina
- Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK
- Department of Clinical and Experimental Medicine, School of Biosciences and Medicine, University of Surrey, Guildford, UK
| | - Karla Sofia Gutiérrez González
- Department of Epidemiology, Erasmus Medical Center, Rotterdam, the Netherlands
- Department of Molecular Diagnostics, Clinical Laboratory, Clinica Biblica Hospital, San José, Costa Rica
| | - Zhanna Balkhiyarova
- Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK
- Department of Clinical and Experimental Medicine, School of Biosciences and Medicine, University of Surrey, Guildford, UK
- People-Centred Artificial Intelligence Institute, University of Surrey, Guildford, UK
| | - Alessia Faggian
- Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK
- Department of Clinical and Experimental Medicine, School of Biosciences and Medicine, University of Surrey, Guildford, UK
- Laboratory for Artificial Biology, Department of Cellular, Computational and Integrative Biology, University of Trento, Trento, Italy
| | - Jared G Maina
- Department of Clinical and Experimental Medicine, School of Biosciences and Medicine, University of Surrey, Guildford, UK
- UMR 8199-EGID, Institut Pasteur de Lille, CNRS, University of Lille, Lille, France
| | - Shiqian Chen
- Section of Endocrinology and Investigative Medicine, Imperial College London, London, UK
| | - Petar V Todorov
- Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, Denmark
| | - Sodbo Sharapov
- Laboratory of Glycogenomics, Institute of Cytology and Genetics SD RAS, Novosibirsk, Russia
- MSU Institute for Artificial Intelligence, Lomonosov Moscow State University, Moscow, Russia
| | - Alessia David
- Centre for Bioinformatics and System Biology, Department of Life Sciences, Imperial College London, London, UK
| | - Letizia Marullo
- Department of Evolutionary Biology, Genetic Section, University of Ferrara, Ferrara, Italy
| | - Reedik Mägi
- Estonian Genome Centre, Institute of Genomics, University of Tartu, Tartu, Estonia
| | - Roxana-Maria Rujan
- Centre for Sports, Exercise and Life Sciences, Coventry University, Conventry, UK
| | - Emma Ahlqvist
- Lund University Diabetes Centre, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden
| | | | - Ηe Gao
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK
| | - Εvangelos Εvangelou
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK
- Department of Hygiene and Epidemiology, University of Ioannina Medical School, Ioannina, Greece
| | - Beben Benyamin
- Australian Centre for Precision Health, University of South Australia, Adelaide, South Australia, Australia
- Allied Health and Human Performance, University of South Australia, Adelaide, South Australia, Australia
- South Australian Health and Medical Research Institute, Adelaide, South Australia, Australia
| | - Robert A Scott
- MRC Epidemiology Unit, Institute of Metabolic Science, University of Cambridge, Cambridge, UK
| | - Aaron Isaacs
- Department of Epidemiology, Erasmus Medical Center, Rotterdam, the Netherlands
- CARIM School for Cardiovascular Diseases and Maastricht Centre for Systems Biology (MaCSBio), Maastricht University, Maastricht, the Netherlands
- Department of Physiology, Maastricht University, Maastricht, the Netherlands
| | - Jing Hua Zhao
- Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK
| | - Sara M Willems
- Department of Epidemiology, Erasmus Medical Center, Rotterdam, the Netherlands
| | - Toby Johnson
- Clinical Pharmacology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK
| | - Christian Gieger
- Research Unit of Molecular Epidemiology, Institute of Epidemiology, Helmholtz Zentrum München Research Center for Environmental Health, Neuherberg, Germany
- Institute of Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany
- German Center for Diabetes Research (DZD), Neuherberg, Germany
| | - Harald Grallert
- Research Unit of Molecular Epidemiology, Institute of Epidemiology, Helmholtz Zentrum München Research Center for Environmental Health, Neuherberg, Germany
- German Center for Diabetes Research (DZD), Neuherberg, Germany
| | - Christa Meisinger
- Epidemiology, Faculty of Medicine, University of Augsburg, Augsburg, Germany
| | - Martina Müller-Nurasyid
- Institute of Genetic Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany
- IBE, Faculty of Medicine, LMU Munich, Munich, Germany
- Institute of Medical Biostatistics, Epidemiology and Informatics (IMBEI), University Medical Center, Johannes Gutenberg University, Mainz, Germany
- Department of Medicine I, University Hospital Grosshadern, Ludwig-Maximilians-University, Munich, Germany
| | - Rona J Strawbridge
- Cardiovascular Medicine Unit, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden
- Center for Molecular Medicine, Karolinska University Hospital Solna, Stockholm, Sweden
- School of Health and Wellbeing, University of Glasgow, Glasgow, UK
| | - Anuj Goel
- Wellcome Centre for Human Genetics, University of Oxford, Oxford, UK
- Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, UK
| | - Denis Rybin
- Department of Biostatistics, Boston University School of Public Health, Boston, MA, USA
| | - Eva Albrecht
- Institute of Genetic Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany
| | - Anne U Jackson
- Department of Biostatistics and Center for Statistical Genetics, University of Michigan, Ann Arbor, MI, USA
| | - Heather M Stringham
- Department of Biostatistics and Center for Statistical Genetics, University of Michigan, Ann Arbor, MI, USA
| | | | - Eric Farber-Eger
- Vanderbilt Institute for Clinical and Translational Research and Vanderbilt Translational and Clinical Cardiovascular Research Center, Nashville, TN, USA
| | | | - André G Uitterlinden
- Department of Epidemiology, Erasmus Medical Center, Rotterdam, the Netherlands
- Department of Internal Medicine, Erasmus Medical Center, Rotterdam, the Netherlands
| | - Patricia B Munroe
- Clinical Pharmacology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK
- NIHR Barts Cardiovascular Biomedical Research Centre, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK
| | - Morris J Brown
- Clinical Pharmacology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK
| | - Julian Schmidberger
- Department of Internal Medicine I, Ulm University Medical Centre, Ulm, Germany
| | - Oddgeir Holmen
- Department of Public Health and General Practice, Norwegian University of Science and Technology, Trondheim, Norway
| | - Barbara Thorand
- Institute of Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany
- German Center for Diabetes Research (DZD), Neuherberg, Germany
| | - Kristian Hveem
- K G Jebsen Centre for Genetic Epdiemiology, Department of Public Health and General Practice, Norwegian University of Science and Technology, Trondheim, Norway
| | - Tom Wilsgaard
- Department of Community Medicine, Faculty of Health Sciences, University of Tromsø, Tromsø, Norway
- Department of Clinical Medicine, Faculty of Health Sciences, University of Tromsø, Tromsø, Norway
| | - Karen L Mohlke
- Department of Genetics, University of North Carolina, Chapel Hill, NC, USA
| | - Zhe Wang
- The Charles Bronfman Institute for Personalized Medicine, Icahn School of Medicine at Mount Sinai, New York City, NY, USA
| | - Aleksey Shmeliov
- Department of Clinical and Experimental Medicine, School of Biosciences and Medicine, University of Surrey, Guildford, UK
| | - Marcel den Hoed
- The Beijer Laboratory and Department of Immunology, Genetics and Pathology, Uppsala University and SciLifeLab, Uppsala, Sweden
| | - Ruth J F Loos
- Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, Denmark
- The Charles Bronfman Institute for Personalized Medicine, Icahn School of Medicine at Mount Sinai, New York City, NY, USA
- The Mindich Child Health and Development Institute, Icahn School of Medicine at Mount Sinai, New York City, NY, USA
| | - Wolfgang Kratzer
- Department of Internal Medicine I, Ulm University Medical Centre, Ulm, Germany
| | - Mark Haenle
- Department of Internal Medicine I, Ulm University Medical Centre, Ulm, Germany
| | - Wolfgang Koenig
- Deutsches Herzzentrum München, Technische Universität München, Munich, Germany
- German Centre for Cardiovascular Research (DZHK), Partner Site Munich Heart Alliance, Munich, Germany
- Institute of Epidemiology and Medical Biometry, University of Ulm, Ulm, Germany
| | - Bernhard O Boehm
- Lee Kong Chian School of Medicine, Nanyang Technological University Singapore, Singapore and Department of Endocrinology, Tan Tock Seng Hospital, Singapore City, Singapore
| | - Tricia M Tan
- Section of Endocrinology and Investigative Medicine, Imperial College London, London, UK
| | - Alejandra Tomas
- Section of Cell Biology and Functional Genomics, Imperial College London, London, UK
| | - Victoria Salem
- Department of Bioengineering, Imperial College London, South Kensington Campus, London, UK
| | - Inês Barroso
- Exeter Centre of Excellence for Diabetes Research (EXCEED), University of Exeter Medical School, Exeter, UK
| | - Jaakko Tuomilehto
- Public Health Promotion Unit, Finnish Institute for Health and Welfare, Helsinki, Finland
- Department of Public Health, University of Helsinki, Helsinki, Finland
- Diabetes Research Unit, King Abdulaziz University, Jeddah, Saudi Arabia
| | - Michael Boehnke
- Department of Biostatistics and Center for Statistical Genetics, University of Michigan, Ann Arbor, MI, USA
| | - Jose C Florez
- Center for Genomic Medicine and Diabetes Unit, Massachusetts General Hospital, Boston, MA, USA
- Programs in Metabolism and Medical and Population Genetics, Broad Institute, Cambridge, MA, USA
- Department of Medicine, Harvard Medical School, Boston, MA, USA
| | - Anders Hamsten
- Cardiovascular Medicine Unit, Department of Medicine, Solna, Karolinska Institutet, Stockholm, Sweden
- Center for Molecular Medicine, Karolinska University Hospital Solna, Stockholm, Sweden
| | - Hugh Watkins
- Wellcome Centre for Human Genetics, University of Oxford, Oxford, UK
- Cardiovascular Medicine, Radcliffe Department of Medicine, University of Oxford, Oxford, UK
| | - Inger Njølstad
- Department of Community Medicine, Faculty of Health Sciences, University of Tromsø, Tromsø, Norway
- Department of Clinical Medicine, Faculty of Health Sciences, University of Tromsø, Tromsø, Norway
| | - H-Erich Wichmann
- Institute of Epidemiology, Helmholtz Zentrum München, German Research Center for Environmental Health, Neuherberg, Germany
| | - Mark J Caulfield
- Clinical Pharmacology, William Harvey Research Institute, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK
- NIHR Barts Cardiovascular Biomedical Research Centre, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London, UK
| | - Kay-Tee Khaw
- Department of Public Health and Primary Care, University of Cambridge, Cambridge, UK
| | - Cornelia M van Duijn
- Department of Epidemiology, Erasmus Medical Center, Rotterdam, the Netherlands
- Centre for Medical Systems Biology, Leiden, the Netherlands
- Nuffield Department of Population Health, University of Oxford, Oxford, UK
| | - Albert Hofman
- Department of Epidemiology, Erasmus Medical Center, Rotterdam, the Netherlands
- Netherlands Consortium for Healthy Ageing, the Hague, the Netherlands
| | - Nicholas J Wareham
- MRC Epidemiology Unit, Institute of Metabolic Science, University of Cambridge, Cambridge, UK
| | - Claudia Langenberg
- MRC Epidemiology Unit, Institute of Metabolic Science, University of Cambridge, Cambridge, UK
- Computational Medicine, Berlin Institute of Health at Charité-Universitätsmedizin Berlin, Berlin, Germany
- Precision Healthcare University Research Institute, Queen Mary University of London, London, UK
| | - John B Whitfield
- QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia
| | - Nicholas G Martin
- QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia
| | - Grant Montgomery
- QIMR Berghofer Medical Research Institute, Brisbane, Queensland, Australia
- Institute for Molecular Bioscience, The University of Queensland, St Lucia, Queensland, Australia
| | - Chiara Scapoli
- Department of Life Sciences and Biotechnology, University of Ferrara, Ferrara, Italy
| | - Ioanna Tzoulaki
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK
- Department of Hygiene and Epidemiology, University of Ioannina Medical School, Ioannina, Greece
| | - Paul Elliott
- Department of Epidemiology and Biostatistics, School of Public Health, Imperial College London, London, UK
- MRC Centre for Environment and Health, Imperial College London, London, UK
- National Institute for Health Research Imperial College London Biomedical Research Centre, Imperial College London, London, UK
| | - Unnur Thorsteinsdottir
- deCODE genetics/Amgen, Inc., Reykjavik, Iceland
- Faculty of Medicine, University of Iceland, Reykjavík, Iceland
| | - Kari Stefansson
- deCODE genetics/Amgen, Inc., Reykjavik, Iceland
- Faculty of Medicine, University of Iceland, Reykjavík, Iceland
| | - Evan L Brittain
- Vanderbilt University Medical Center and the Vanderbilt Translational and Clinical Cardiovascular Research Center, Nashville, TN, USA
| | - Mark I McCarthy
- Wellcome Centre for Human Genetics, University of Oxford, Oxford, UK
- Oxford Centre for Diabetes, Endocrinology and Metabolism, University of Oxford, Oxford, UK
- Genentech, South San Francisco, CA, USA
| | - Philippe Froguel
- Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK
- UMR 8199-EGID, Institut Pasteur de Lille, CNRS, University of Lille, Lille, France
| | - Patrick M Sexton
- Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria, Australia
- ARC Centre for Cryo-Electron Microscopy of Membrane Proteins, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria, Australia
| | - Denise Wootten
- Drug Discovery Biology, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria, Australia
- ARC Centre for Cryo-Electron Microscopy of Membrane Proteins, Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria, Australia
| | - Leif Groop
- Lund University Diabetes Centre, Department of Clinical Sciences Malmö, Lund University, Malmö, Sweden
- Finnish Institute for Molecular Medicine (FIMM), Helsinki University, Helsinki, Finland
| | - Josée Dupuis
- Department of Biostatistics, Boston University School of Public Health, Boston, MA, USA
- Department of Epidemiology, Biostatistics and Occupational Health, McGill University, Montreal, Quebec, Canada
| | - James B Meigs
- Programs in Metabolism and Medical and Population Genetics, Broad Institute, Cambridge, MA, USA
- Department of Medicine, Harvard Medical School, Boston, MA, USA
- Division of General Internal Medicine, Massachusetts General Hospital, Boston, MA, USA
| | - Giuseppe Deganutti
- Centre for Sports, Exercise and Life Sciences, Coventry University, Conventry, UK
| | - Ayse Demirkan
- Department of Clinical and Experimental Medicine, School of Biosciences and Medicine, University of Surrey, Guildford, UK
- People-Centred Artificial Intelligence Institute, University of Surrey, Guildford, UK
- Department of Genetics, University Medical Center Groningen, Groningen, the Netherlands
| | - Tune H Pers
- Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, Denmark
| | - Christopher A Reynolds
- Centre for Sports, Exercise and Life Sciences, Coventry University, Conventry, UK
- School of Life Sciences, University of Essex, Colchester, UK
| | - Yurii S Aulchenko
- Department of Epidemiology, Erasmus Medical Center, Rotterdam, the Netherlands
- Laboratory of Glycogenomics, Institute of Cytology and Genetics SD RAS, Novosibirsk, Russia
- MSU Institute for Artificial Intelligence, Lomonosov Moscow State University, Moscow, Russia
| | - Marika A Kaakinen
- Department of Metabolism, Digestion and Reproduction, Imperial College London, London, UK.
- Department of Clinical and Experimental Medicine, School of Biosciences and Medicine, University of Surrey, Guildford, UK.
- People-Centred Artificial Intelligence Institute, University of Surrey, Guildford, UK.
| | - Ben Jones
- Section of Endocrinology and Investigative Medicine, Imperial College London, London, UK.
| | - Inga Prokopenko
- Department of Clinical and Experimental Medicine, School of Biosciences and Medicine, University of Surrey, Guildford, UK.
- People-Centred Artificial Intelligence Institute, University of Surrey, Guildford, UK.
- UMR 8199-EGID, Institut Pasteur de Lille, CNRS, University of Lille, Lille, France.
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Cai YW, Zhang HF, Gao JW, Cai ZX, Cai JW, Gao QY, Chen ZT, Liao GH, Zeng CR, Chen N, Liu PM, Wang JF, Chen YX. Serum albumin and risk of incident diabetes and diabetic microvascular complications in the UK Biobank cohort. DIABETES & METABOLISM 2023; 49:101472. [PMID: 37678759 DOI: 10.1016/j.diabet.2023.101472] [Citation(s) in RCA: 8] [Impact Index Per Article: 4.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 02/25/2023] [Revised: 07/18/2023] [Accepted: 07/25/2023] [Indexed: 09/09/2023]
Abstract
AIM To examine the associations between serum albumin and the incidences of diabetes and diabetic microvascular complications in participants of the UK Biobank cohort. METHODS There were 398,146 participants without diabetes and 30,952 patients with diabetes from the UK Biobank cohort included in this study. Multivariate-adjusted Cox proportional hazard models were used to analyze the association of albumin with the incidences of diabetes and diabetic microvascular complications. Mendelian randomization (MR) analysis was used to determine the genetic relationships between serum albumin and diabetes. RESULTS After a median 12.90 years follow-up, 14,710 participants developed incident diabetes (58.83 ± 7.52 years, 56.10% male). After multivariate adjustment, serum albumin was inversely associated with incident diabetes: hazard ratio (HR) [95% confidence interval] per 10 g/l increase 0.88 [0.82;0.94]. MR analyses suggested a potential genetic influence of serum albumin on diabetes in both the UK Biobank and the FinnGen consortium: odds ratios (ORs) [95% confidence interval per 1 g/l increase 0.99 [0.98;1.00] and 0.78 [0.67;0.92], respectively. In patients with diabetes, higher serum albumin levels were significantly associated with lower risk for diabetic microvascular complications. Specifically, per 10 g/l increase in serum albumin, the HRs for diabetic nephropathy, ophthalmopathy, and neuropathy were 0.42 [0.30;0.58], 0.61 [0.52;0.72], and 0.67 [0.51;0.88], respectively. CONCLUSION In this large prospective study, serum levels of albumin were inversely associated with the incidences of diabetes and diabetic microvascular complications. These findings underscore the importance of maintaining optimal nutrient status in reducing the risk of diabetes and its complications.
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Affiliation(s)
- Yang-Wei Cai
- Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China
| | - Hai-Feng Zhang
- Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China
| | - Jing-Wei Gao
- Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China
| | - Zhao-Xi Cai
- Department of Radiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China
| | - Jie-Wen Cai
- Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China
| | - Qing-Yuan Gao
- Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China
| | - Zhi-Teng Chen
- Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China
| | - Guang-Hong Liao
- Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China
| | - Chuan-Rui Zeng
- Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China
| | - Nuo Chen
- Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China
| | - Pin-Ming Liu
- Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
| | - Jing-Feng Wang
- Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
| | - Yang-Xin Chen
- Department of Cardiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China; Guangdong Province Key Laboratory of Arrhythmia and Electrophysiology, Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.
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Sooriyaarachchi P, Jayawardena R, Pavey T, King NA. The effect of shift work on different hematological parameters among healthcare workers. Chronobiol Int 2023; 40:918-925. [PMID: 37424389 DOI: 10.1080/07420528.2023.2231079] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/11/2023] [Revised: 06/01/2023] [Accepted: 06/24/2023] [Indexed: 07/11/2023]
Abstract
Shift workers frequently experience alterations in their circadian rhythms, which are correlated with variations in hematological parameters. Changes in blood cells may be related to an individual's health status. Therefore, this study aimed to compare the relationship between shift work and changes in blood cells among a group of healthcare workers in Sri Lanka. A comparative cross-sectional study was conducted among healthcare workers, recruited by a stratified random sampling technique. Socio-demographic data were collected using a structured questionnaire. Venous blood samples were obtained and analyzed for the determination of total and differential blood cell counts. Descriptive statistics were used for the analysis of sociodemographic and hematological parameters. A sample of 37-day workers and 39 shift workers were included in the analysis. The mean ages (years) were not significantly different between the groups (36.8 ± 10.8 vs 39.1 ± 12.0; P = 0.371). Shift employees showed a significantly higher total mean white blood cell count (WBC) of 7548.75 mm-3 compared to day workers' 6869.19 mm-3 (P = 0.027). They also had higher mean absolute counts for all different WBC types (Neutrophils: 3949.2 vs 3557.7 , Lymphocyte: 2756.5 vs 2614.2 , Eosinophil: 317.6 vs 233.4 , Monocytes: 491.63 vs 432.51 , Basophils: 31.68 vs 29.22 ). Shift employees exhibited higher WBC counts than day workers at the same level of work experience. The length of shift work exposure revealed a positive link with neutrophil (r = 0.225 ) and eosinophil counts (r = 0.262 ), whereas these correlations were negative for day workers. Shift workers were associated with higher WBC counts in healthcare workers compared to their day-working counterparts.
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Affiliation(s)
- Piumika Sooriyaarachchi
- Faculty of Health, School of Exercise and Nutrition Sciences, Queensland University of Technology (QUT), Brisbane, Queensland, Australia
- Health and Wellness Unit, Faculty of Medicine, University of Colombo, Colombo, Sri Lanka
| | - Ranil Jayawardena
- Faculty of Health, School of Exercise and Nutrition Sciences, Queensland University of Technology (QUT), Brisbane, Queensland, Australia
- Department of Physiology, Faculty of Medicine, University of Colombo, Colombo, Sri Lanka
| | - Toby Pavey
- Faculty of Health, School of Exercise and Nutrition Sciences, Queensland University of Technology (QUT), Brisbane, Queensland, Australia
| | - Neil A King
- Faculty of Health, School of Exercise and Nutrition Sciences, Queensland University of Technology (QUT), Brisbane, Queensland, Australia
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Liberale L, Kraler S, Puspitasari YM, Bonetti NR, Akhmedov A, Ministrini S, Montecucco F, Marx N, Lehrke M, Hartmann NUK, Beer JH, Wenzl FA, Paneni F, Lüscher TF, Camici GG. SGLT-2 inhibition by empagliflozin has no effect on experimental arterial thrombosis in a murine model of low-grade inflammation. Cardiovasc Res 2023; 119:843-856. [PMID: 35993135 DOI: 10.1093/cvr/cvac126] [Citation(s) in RCA: 6] [Impact Index Per Article: 3.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/04/2022] [Accepted: 05/04/2022] [Indexed: 11/14/2022] Open
Abstract
AIMS Low-grade inflammation couples dysmetabolic states to insulin resistance and atherosclerotic cardiovascular (CV) disease (ASCVD). Selective sodium-glucose co-transporter 2 (SGLT-2) inhibition by empagliflozin improves clinical outcomes in patients with ASCVD independently of its glucose lowering effects. Yet, its mechanism of action remains largely undetermined. Here, we aimed to test whether empagliflozin affects arterial thrombus formation in baseline (BSL) conditions or low-grade inflammatory states, a systemic milieu shared among patients with ASCVD. METHODS AND RESULTS Sixteen-week-old C57BL/6 mice were randomly assigned to acute administration of empagliflozin (25 mg/kg body weight) or vehicle, of which a subgroup was pre-treated biweekly over 4 weeks with super-low-dose lipopolysaccharide (LPS; 5 ng/kg body weight), before carotid thrombosis was induced by photochemical injury. The between-group difference in Doppler-flow probe detected time-to-occlusion remained within the predefined equivalence margin (Δ = |10.50|), irrespective of low-grade inflammation (95% confidence interval, -9.82 to 8.85 and -9.20 to 9.69), while glucose dropped by 1.64 and 4.84 mmoL/L, respectively. Ex vivo platelet aggregometry suggested similar activation status, corroborated by unchanged circulating platelet-factor 4 plasma levels. In concert, carotid PAI-1 expression and tissue factor (TF) activity remained unaltered upon SGLT-2 inhibition, and no difference in plasma D-dimer levels was detected, suggesting comparable coagulation cascade activation and fibrinolytic activity. In human aortic endothelial cells pre-treated with LPS, empagliflozin neither changed TF activity nor PAI-1 expression. Accordingly, among patients with established ASCVD or at high CV risk randomized to a daily dose of 10 mg empagliflozin signatures of thrombotic (i.e. TF) and fibrinolytic activity (i.e. PAI-1) remained unchanged, while plasma glucose declined significantly during 3 months of follow-up. CONCLUSION SGLT-2 inhibition by empagliflozin does not impact experimental arterial thrombus formation, neither under BSL conditions nor during sustained low-grade inflammation, and has no impact on proxies of thrombotic/fibrinolytic activity in patients with ASCVD. The beneficial pleiotropic effects of empagliflozin are likely independent of pathways mediating arterial thrombosis.
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Affiliation(s)
- Luca Liberale
- Center for Molecular Cardiology, University of Zurich, Wagistrasse 12, 8952 Schlieren, Switzerland
- First Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa, 16132 Genoa, Italy
| | - Simon Kraler
- Center for Molecular Cardiology, University of Zurich, Wagistrasse 12, 8952 Schlieren, Switzerland
| | - Yustina M Puspitasari
- Center for Molecular Cardiology, University of Zurich, Wagistrasse 12, 8952 Schlieren, Switzerland
| | - Nicole R Bonetti
- University Heart Center, Department of Cardiology, University Hospital Zurich, 8091 Zurich, Switzerland
| | - Alexander Akhmedov
- Center for Molecular Cardiology, University of Zurich, Wagistrasse 12, 8952 Schlieren, Switzerland
| | - Stefano Ministrini
- Center for Molecular Cardiology, University of Zurich, Wagistrasse 12, 8952 Schlieren, Switzerland
- Internal Medicine, Angiology and Atherosclerosis, Department of Medicine and Surgery, University of Perugia, 06123 Perugia, Italy
| | - Fabrizio Montecucco
- First Clinic of Internal Medicine, Department of Internal Medicine, University of Genoa, 16132 Genoa, Italy
- IRCCS Ospedale Policlinico San Martino Genoa - Italian Cardiovascular Network, 16132 Genoa, Italy
| | - Nikolaus Marx
- Department of Internal Medicine I, University Hospital Aachen, RWTH, 52074 Aachen, Germany
| | - Michael Lehrke
- Department of Internal Medicine I, University Hospital Aachen, RWTH, 52074 Aachen, Germany
| | - Niels-Ulrik K Hartmann
- Department of Internal Medicine I, University Hospital Aachen, RWTH, 52074 Aachen, Germany
| | - Jürg H Beer
- Center for Molecular Cardiology, University of Zurich, Wagistrasse 12, 8952 Schlieren, Switzerland
- Department of Internal Medicine, Cantonal Hospital of Baden, 5404 Baden, Switzerland
| | - Florian A Wenzl
- Center for Molecular Cardiology, University of Zurich, Wagistrasse 12, 8952 Schlieren, Switzerland
| | - Francesco Paneni
- Center for Molecular Cardiology, University of Zurich, Wagistrasse 12, 8952 Schlieren, Switzerland
- University Heart Center, Department of Cardiology, University Hospital Zurich, 8091 Zurich, Switzerland
- Department of Research and Education, University Hospital Zurich, 8091 Zurich, Switzerland
| | - Thomas F Lüscher
- Center for Molecular Cardiology, University of Zurich, Wagistrasse 12, 8952 Schlieren, Switzerland
- Royal Brompton and Harefield Hospitals and Imperial College, SW3 6NP London, UK
| | - Giovanni G Camici
- Center for Molecular Cardiology, University of Zurich, Wagistrasse 12, 8952 Schlieren, Switzerland
- University Heart Center, Department of Cardiology, University Hospital Zurich, 8091 Zurich, Switzerland
- Department of Research and Education, University Hospital Zurich, 8091 Zurich, Switzerland
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Hayden MR. Overview and New Insights into the Metabolic Syndrome: Risk Factors and Emerging Variables in the Development of Type 2 Diabetes and Cerebrocardiovascular Disease. Medicina (B Aires) 2023; 59:medicina59030561. [PMID: 36984562 PMCID: PMC10059871 DOI: 10.3390/medicina59030561] [Citation(s) in RCA: 22] [Impact Index Per Article: 11.0] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/05/2023] [Revised: 03/04/2023] [Accepted: 03/10/2023] [Indexed: 03/16/2023] Open
Abstract
Metabolic syndrome (MetS) is considered a metabolic disorder that has been steadily increasing globally and seems to parallel the increasing prevalence of obesity. It consists of a cluster of risk factors which traditionally includes obesity and hyperlipidemia, hyperinsulinemia, hypertension, and hyperglycemia. These four core risk factors are associated with insulin resistance (IR) and, importantly, the MetS is known to increase the risk for developing cerebrocardiovascular disease and type 2 diabetes mellitus. The MetS had its early origins in IR and syndrome X. It has undergone numerous name changes, with additional risk factors and variables being added over the years; however, it has remained as the MetS worldwide for the past three decades. This overview continues to add novel insights to the MetS and suggests that leptin resistance with hyperleptinemia, aberrant mitochondrial stress and reactive oxygen species (ROS), impaired folate-mediated one-carbon metabolism with hyperhomocysteinemia, vascular stiffening, microalbuminuria, and visceral adipose tissues extracellular vesicle exosomes be added to the list of associated variables. Notably, the role of a dysfunctional and activated endothelium and deficient nitric oxide bioavailability along with a dysfunctional and attenuated endothelial glycocalyx, vascular inflammation, systemic metainflammation, and the important role of ROS and reactive species interactome are discussed. With new insights and knowledge regarding the MetS comes the possibility of new findings through further research.
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Affiliation(s)
- Melvin R Hayden
- Department of Internal Medicine, Endocrinology Diabetes and Metabolism, Diabetes and Cardiovascular Disease Center, University of Missouri School of Medicine, One Hospital Drive, Columbia, MO 65211, USA
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Liu H, Ju A, Dong X, Luo Z, Tang J, Ma B, Fu Y, Luo Y. Young and undamaged recombinant albumin alleviates T2DM by improving hepatic glycolysis through EGFR and protecting islet β cells in mice. J Transl Med 2023; 21:89. [PMID: 36747238 PMCID: PMC9903539 DOI: 10.1186/s12967-023-03957-3] [Citation(s) in RCA: 4] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/19/2022] [Accepted: 02/01/2023] [Indexed: 02/08/2023] Open
Abstract
BACKGROUND Albumin is the most abundant protein in serum and serves as a transporter of free fatty acids (FFA) in blood vessels. In type 2 diabetes mellitus (T2DM) patients, the reduced serum albumin level is a risk factor for T2DM development and progression, although this conclusion is controversial. Moreover, there is no study on the effects and mechanisms of albumin administration to relieve T2DM. We examined whether the administration of young and undamaged recombinant albumin can alleviate T2DM in mice. METHODS The serum albumin levels and metabolic phenotypes including fasting blood glucose, glucose tolerance tests, and glucose-stimulated insulin secretion were studied in db/db mice or diet-induced obesity mice treated with saline or young, undamaged, and ultrapure rMSA. Apoptosis assays were performed at tissue and cell levels to determine the function of rMSA on islet β cell protection. Metabolic flux and glucose uptake assays were employed to investigate metabolic changes in saline-treated or rMSA-treated mouse hepatocytes and compared their sensitivity to insulin treatments. RESULTS In this study, treatment of T2DM mice with young, undamaged, and ultrapure recombinant mouse serum albumin (rMSA) increased their serum albumin levels, which resulted in a reversal of the disease including reduced fasting blood glucose levels, improved glucose tolerance, increased glucose-stimulated insulin secretion, and alleviated islet atrophy. At the cellular level, rMSA improved glucose uptake and glycolysis in hepatocytes. Mechanistically, rMSA reduced the binding between CAV1 and EGFR to increase EGFR activation leading to PI3K-AKT activation. Furthermore, rMSA extracellularly reduced the rate of fatty acid uptake by islet β-cells, which relieved the accumulation of intracellular ceramide, endoplasmic reticulum stress, and apoptosis. This study provided the first clear demonstration that injections of rMSA can alleviate T2DM in mice. CONCLUSION Our study demonstrates that increasing serum albumin levels can promote glucose homeostasis and protect islet β cells, which alleviates T2DM.
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Affiliation(s)
- Hongyi Liu
- grid.12527.330000 0001 0662 3178School of Life Sciences, Tsinghua University, Beijing, 100084 China ,grid.452723.50000 0004 7887 9190Tsinghua-Peking Joint Center for Life Sciences, Beijing, 100084 China ,The National Engineering Research Center for Protein Technology, Beijing, 100084 China ,Beijing Key Laboratory for Protein Therapeutics, Beijing, 100084 China
| | - Anji Ju
- grid.12527.330000 0001 0662 3178School of Life Sciences, Tsinghua University, Beijing, 100084 China ,The National Engineering Research Center for Protein Technology, Beijing, 100084 China ,Beijing Key Laboratory for Protein Therapeutics, Beijing, 100084 China
| | - Xuan Dong
- grid.12527.330000 0001 0662 3178School of Life Sciences, Tsinghua University, Beijing, 100084 China ,The National Engineering Research Center for Protein Technology, Beijing, 100084 China ,Beijing Key Laboratory for Protein Therapeutics, Beijing, 100084 China
| | - Zongrui Luo
- grid.12527.330000 0001 0662 3178School of Life Sciences, Tsinghua University, Beijing, 100084 China ,The National Engineering Research Center for Protein Technology, Beijing, 100084 China ,Beijing Key Laboratory for Protein Therapeutics, Beijing, 100084 China
| | - Jiaze Tang
- grid.12527.330000 0001 0662 3178School of Life Sciences, Tsinghua University, Beijing, 100084 China ,The National Engineering Research Center for Protein Technology, Beijing, 100084 China ,Beijing Key Laboratory for Protein Therapeutics, Beijing, 100084 China
| | - Boyuan Ma
- grid.12527.330000 0001 0662 3178School of Life Sciences, Tsinghua University, Beijing, 100084 China ,The National Engineering Research Center for Protein Technology, Beijing, 100084 China ,Beijing Key Laboratory for Protein Therapeutics, Beijing, 100084 China
| | - Yan Fu
- School of Life Sciences, Tsinghua University, Beijing, 100084, China. .,The National Engineering Research Center for Protein Technology, Beijing, 100084, China. .,Beijing Key Laboratory for Protein Therapeutics, Beijing, 100084, China. .,School of Life Sciences, Tsinghua University, Beijing, 100084, China.
| | - Yongzhang Luo
- School of Life Sciences, Tsinghua University, Beijing, 100084, China. .,Tsinghua-Peking Joint Center for Life Sciences, Beijing, 100084, China. .,The National Engineering Research Center for Protein Technology, Beijing, 100084, China. .,Beijing Key Laboratory for Protein Therapeutics, Beijing, 100084, China. .,School of Life Sciences, Tsinghua University, Beijing, 100084, China.
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Mazza E, Calesella F, Paolini M, di Pasquasio C, Poletti S, Lorenzi C, Falini A, Zanardi R, Colombo C, Benedetti F. Insulin resistance disrupts white matter microstructure and amplitude of functional spontaneous activity in bipolar disorder. Bipolar Disord 2023; 25:32-42. [PMID: 36377438 DOI: 10.1111/bdi.13270] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/16/2022]
Abstract
BACKGROUND Bipolar disorder (BD) is linked to several structural and functional brain alterations. In addition, BD patients have a three-fold increased risk of developing insulin resistance, which is associated with neural changes and poorer BD outcomes. Therefore, we investigated the effects of insulin and two derived measures (insulin resistance and sensitivity) on white matter (WM) microstructure, resting-state (rs) functional connectivity (FC), and fractional amplitude of low-frequency fluctuation (fALFF). METHODS BD patients (n = 92) underwent DTI acquisition, and a subsample (n = 22) underwent rs-fMRI. Blood samples were collected to determine insulin and glucose levels. The Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) and quantitative insulin sensitivity check index (QUICKI) were computed. DTI data were analyzed via tract-based spatial statistics and threshold-free cluster enhancement. From rs-fMRI data, both ROI-to-ROI FC matrices and fALFF maps were extracted. RESULTS Insulin showed a widespread negative association with fractional anisotropy (FA) and a positive effect on radial diffusivity (RD) and mean diffusivity (MD). HOMA-IR exerted a significant effect on RD in the right superior longitudinal fasciculus, whereas QUICKI was positively associated with FA and negatively with RD and MD in the left superior longitudinal fasciculus, left anterior corona radiata, and forceps minor. fALFF was negatively modulated by insulin and HOMA-IR and positively associated with QUICKI in the precuneus. No significant results were found in the ROI-to-ROI analysis. CONCLUSION Our findings suggest that WM microstructure and functional alterations might underlie the effect of IR on BD pathophysiology, even if the causal mechanisms need to be further investigated.
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Affiliation(s)
- Elena Mazza
- Vita-Salute San Raffaele University, Milan, Italy.,Psychiatry and Clinical Psychobiology, Division of Neuroscience, Scientific Institute IRCCS Ospedale San Raffaele, Milan, Italy
| | - Federico Calesella
- Vita-Salute San Raffaele University, Milan, Italy.,Psychiatry and Clinical Psychobiology, Division of Neuroscience, Scientific Institute IRCCS Ospedale San Raffaele, Milan, Italy
| | - Marco Paolini
- Vita-Salute San Raffaele University, Milan, Italy.,Psychiatry and Clinical Psychobiology, Division of Neuroscience, Scientific Institute IRCCS Ospedale San Raffaele, Milan, Italy
| | | | - Sara Poletti
- Vita-Salute San Raffaele University, Milan, Italy.,Psychiatry and Clinical Psychobiology, Division of Neuroscience, Scientific Institute IRCCS Ospedale San Raffaele, Milan, Italy
| | - Cristina Lorenzi
- Psychiatry and Clinical Psychobiology, Division of Neuroscience, Scientific Institute IRCCS Ospedale San Raffaele, Milan, Italy
| | - Andrea Falini
- Vita-Salute San Raffaele University, Milan, Italy.,C.E.R.M.A.C. (Centro di Eccellenza Risonanza Magnetica ad Alto Campo), University Vita-Salute San Raffaele, Milan, Italy
| | - Raffaella Zanardi
- Vita-Salute San Raffaele University, Milan, Italy.,Mood Disorders Unit, IRCCS Scientific Institute Ospedale San Raffaele, Milano, Italy
| | - Cristina Colombo
- Vita-Salute San Raffaele University, Milan, Italy.,Mood Disorders Unit, IRCCS Scientific Institute Ospedale San Raffaele, Milano, Italy
| | - Francesco Benedetti
- Vita-Salute San Raffaele University, Milan, Italy.,Psychiatry and Clinical Psychobiology, Division of Neuroscience, Scientific Institute IRCCS Ospedale San Raffaele, Milan, Italy
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Andreozzi F, Di Fatta C, Spiga R, Mannino GC, Mancuso E, Averta C, De Caro C, Tallarico M, Leo A, Citraro R, Russo E, De Sarro G, Sesti G. Glucagon induces the hepatic expression of inflammatory markers in vitro and in vivo. Diabetes Obes Metab 2023; 25:556-569. [PMID: 36305474 DOI: 10.1111/dom.14902] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 06/21/2022] [Revised: 10/12/2022] [Accepted: 10/24/2022] [Indexed: 02/02/2023]
Abstract
Glucagon exerts multiple hepatic actions, including stimulation of glycogenolysis/gluconeogenesis. The liver plays a crucial role in chronic inflammation by synthesizing proinflammatory molecules, which are thought to contribute to insulin resistance and hyperglycaemia. Whether glucagon affects hepatic expression of proinflammatory cytokines and acute-phase reactants is unknown. Herein, we report a positive relationship between fasting glucagon levels and circulating interleukin (IL)-1β (r = 0.252, p = .042), IL-6 (r = 0.230, p = .026), fibrinogen (r = 0.193, p = .031), complement component 3 (r = 0.227, p = .024) and high sensitivity C-reactive protein (r = 0.230, p = .012) in individuals without diabetes. In CD1 mice, 4-week continuous treatment with glucagon induced a significant increase in circulating IL-1β (p = .02), and IL-6 (p = .001), which was countered by the contingent administration of the glucagon receptor antagonist, GRA-II. Consistent with these results, we detected a significant increase in the hepatic activation of inflammatory pathways, such as expression of NLRP3 (p < .02), and the phosphorylation of nuclear factor kappaB (NF-κB; p < .02) and STAT3 (p < .01). In HepG2 cells, we found that glucagon dose-dependently stimulated the expression of IL-1β (p < .002), IL-6 (p < .002), fibrinogen (p < .01), complement component 3 (p < .01) and C-reactive protein (p < .01), stimulated the activation of NLRP3 inflammasome (p < .01) and caspase-1 (p < .05), induced the phosphorylation of TRAF2 (p < .01), NF-κB (p < .01) and STAT3 (p < .01). Preincubating cells with GRA-II inhibited the ability of glucagon to induce an inflammatory response. Using HepaRG cells, we confirmed the dose-dependent ability of glucagon to stimulate the expression of NLRP3, the phosphorylation of NF-κB and STAT3, in the absence of GRA-II. These results suggest that glucagon has proinflammatory effects that may participate in the pathogenesis of hyperglycaemia and unfavourable cardiometabolic risk profile.
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Affiliation(s)
- Francesco Andreozzi
- Department of Medical and Surgical Sciences, University Magna Graecia of Catanzaro, Catanzaro, Italy
- Research Center for the Prevention and Treatment of Metabolic Diseases (CR METDIS), University Magna Graecia of Catanzaro, Catanzaro, Italy
| | - Concetta Di Fatta
- Department of Medical and Surgical Sciences, University Magna Graecia of Catanzaro, Catanzaro, Italy
| | - Rosangela Spiga
- Department of Medical and Surgical Sciences, University Magna Graecia of Catanzaro, Catanzaro, Italy
| | - Gaia Chiara Mannino
- Department of Medical and Surgical Sciences, University Magna Graecia of Catanzaro, Catanzaro, Italy
| | - Elettra Mancuso
- Department of Medical and Surgical Sciences, University Magna Graecia of Catanzaro, Catanzaro, Italy
| | - Carolina Averta
- Department of Medical and Surgical Sciences, University Magna Graecia of Catanzaro, Catanzaro, Italy
| | - Carmen De Caro
- Department of Science of Health, University Magna Graecia of Catanzaro, Catanzaro, Italy
| | - Martina Tallarico
- Department of Science of Health, University Magna Graecia of Catanzaro, Catanzaro, Italy
| | - Antonio Leo
- Department of Science of Health, University Magna Graecia of Catanzaro, Catanzaro, Italy
| | - Rita Citraro
- Department of Science of Health, University Magna Graecia of Catanzaro, Catanzaro, Italy
| | - Emilio Russo
- Department of Science of Health, University Magna Graecia of Catanzaro, Catanzaro, Italy
| | | | - Giorgio Sesti
- Department of Clinical and Molecular Medicine, University of Rome-Sapienza, Rome, Italy
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Zhao W, Li X, Li X, Peng L, Li Y, Du Y, He J, Qin Y, Zhang H. Significant increase of serum extracellular vesicle-packaged growth differentiation factor 15 in type 2 diabetes mellitus: a cross-sectional study. Eur J Med Res 2023; 28:37. [PMID: 36658625 PMCID: PMC9850700 DOI: 10.1186/s40001-023-01009-6] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/07/2022] [Accepted: 01/11/2023] [Indexed: 01/20/2023] Open
Abstract
BACKGROUND Growth differentiation factor 15 (GDF15) is a stress-inducible factor involved in the inflammatory progression of many complications, including type 2 diabetes mellitus (T2DM). Growing evidence suggests that molecules in extracellular vesicles (EVs) are associated with diabetes or diabetes-related complications. However, the correlation between serum extracellular vesicle-derived growth differentiation factor15 (EV-GDF15) and T2DM is unknown. The aim of this cross-sectional study is to investigate whether serum EV-GDF15 is associated with T2DM incidence. METHODS 116 individuals, including 78 T2DM and 38 non-T2DM, were recruited as participants. The concentrations of serum EV-GDF15 and serum GDF15 were determined by Luminex assay. Serum EVs were obtained by ultracentrifugation. Multivariate stepwise regression analysis was used to determine the association between serum GDF15 levels and fasting plasma glucose (FPG) as well as glycated hemoglobin (HbA1c). The association of serum EV-GDF15 levels with T2DM was determined by multivariate logistic regression analysis. RESULTS Our data showed that the levels of serum EV-GDF15 and serum GDF15 were significantly increased in T2DM patients compared with non-T2DM subjects (EV-GDF15 levels, 13.68 (6.61-23.44) pg/mL vs. 5.56 (3.44-12.09) pg/mL, P < 0.001; and serum GDF15 levels, 1025.49 (677.87-1626.36) pg/mL vs. 675.46 (469.53-919.98) pg/mL, P < 0.001). There was a linear correlation between EV-GDF15 levels and fasting plasma glucose (FPG) and Hemoglobin A1C (HbA1c) levels (normalized β = 0.357, P < 0.001; normalized β = 0.409, P < 0.001, respectively). Elevated levels of EV-GDF15 were accompanied by an increase in the proportion of patients with T2DM (from 47.5 to 78.9%) and a progressive independent association with the incidence of T2DM (from OR = 3.06, 95% CI 1.02-9.19, P = 0.047 to OR = 3.75, 95% CI 1.14-12.26, P = 0.029). Notably, high levels of serum GDF15 plus high levels of serum EV-GDF15 were significantly associated with T2DM more than either alone. CONCLUSION This study elucidated that increased levels of GDF15 in serum EVs were independently associated with T2DM.
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Affiliation(s)
- Wen Zhao
- grid.24696.3f0000 0004 0369 153XBeijing Anzhen Hospital, Beijing Institute of Heart Lung and Blood Vessel Disease, Capital Medical University, No. 2 Anzhen Road, Beijing, 100029 China
| | - Xinwei Li
- grid.24696.3f0000 0004 0369 153XBeijing Anzhen Hospital, Beijing Institute of Heart Lung and Blood Vessel Disease, Capital Medical University, No. 2 Anzhen Road, Beijing, 100029 China
| | - Xinxin Li
- grid.24696.3f0000 0004 0369 153XBeijing Anzhen Hospital, Beijing Institute of Heart Lung and Blood Vessel Disease, Capital Medical University, No. 2 Anzhen Road, Beijing, 100029 China
| | - Lu Peng
- grid.24696.3f0000 0004 0369 153XBeijing Anzhen Hospital, Beijing Institute of Heart Lung and Blood Vessel Disease, Capital Medical University, No. 2 Anzhen Road, Beijing, 100029 China
| | - Yu Li
- grid.24696.3f0000 0004 0369 153XBeijing Anzhen Hospital, Beijing Institute of Heart Lung and Blood Vessel Disease, Capital Medical University, No. 2 Anzhen Road, Beijing, 100029 China
| | - Yunhui Du
- grid.24696.3f0000 0004 0369 153XBeijing Anzhen Hospital, Beijing Institute of Heart Lung and Blood Vessel Disease, Capital Medical University, No. 2 Anzhen Road, Beijing, 100029 China
| | - Jianxun He
- grid.24696.3f0000 0004 0369 153XBeijing Anzhen Hospital Laboratory Department, Beijing Anzhen Hospital, Capital Medical University, Beijing, 100029 China
| | - Yanwen Qin
- grid.24696.3f0000 0004 0369 153XBeijing Anzhen Hospital, Beijing Institute of Heart Lung and Blood Vessel Disease, Capital Medical University, No. 2 Anzhen Road, Beijing, 100029 China
| | - Huina Zhang
- grid.24696.3f0000 0004 0369 153XBeijing Anzhen Hospital, Beijing Institute of Heart Lung and Blood Vessel Disease, Capital Medical University, No. 2 Anzhen Road, Beijing, 100029 China
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Chen YK, Wu PY, Huang JC, Chen SC, Chang JM. Sex difference in the associations among liver function parameters with incident diabetes mellitus in a large Taiwanese population follow-up study. Front Public Health 2023; 10:1081374. [PMID: 36684957 PMCID: PMC9845575 DOI: 10.3389/fpubh.2022.1081374] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/27/2022] [Accepted: 12/12/2022] [Indexed: 01/06/2023] Open
Abstract
Background The prevalence of diabetes mellitus (DM) in Taiwan between 2017 and 2020 was 11.05%, which is higher than the global prevalence (10.5%). Previous studies have shown that patients with DM have higher liver enzyme levels than those without DM. However, it is unclear whether there are sex differences in the association between incident DM and liver function. Therefore, the aim of this longitudinal study was to investigate this issue in a large Taiwanese cohort. Methods We identified 27,026 participants from the Taiwan Biobank, and excluded those with baseline DM (n = 2,637), and those without follow-up data on DM, serum fasting glucose or glycosylated hemoglobin A1c (n = 43). The remaining 24,346 participants (male: 8,334; female: 16,012; mean age 50.5 ± 10.4 years) were enrolled and followed for a median of 4 years. Results Of the enrolled participants, 1,109 (4.6%) had incident DM and 23,237 (95.4%) did not. Multivariable analysis showed that high levels of glutamic-oxaloacetic transaminase (AST) (p < 0.001), glutamic-pyruvic transaminase (ALT) (p < 0.001), albumin (p = 0.003), α-fetoprotein (p = 0.019), and gamma-glutamyl transpeptidase (GGT) (p = 0.001) were significantly associated with incident DM in the male participants. In comparison, high levels of AST (p = 0.010), ALT (p < 0.001), albumin (p = 0.001) and GGT (p < 0.001), and low total bilirubin (p = 0.001) were significantly associated with incident DM in the female participants. There were significant interactions between total bilirubin and sex (p = 0.031), and GGT and sex (p = 0.011) on incident DM. Conclusion In conclusion, liver function parameters were significantly associated with incident DM. Further, there were differences in the associations between the male and female participants.
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Affiliation(s)
- Yi-Kong Chen
- Department of General Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan
| | - Pei-Yu Wu
- Department of Internal Medicine, Kaohsiung Municipal Siaogang Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan
- Division of Nephrology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan
- Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
| | - Jiun-Chi Huang
- Department of Internal Medicine, Kaohsiung Municipal Siaogang Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan
- Division of Nephrology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan
- Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
| | - Szu-Chia Chen
- Department of Internal Medicine, Kaohsiung Municipal Siaogang Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan
- Division of Nephrology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan
- Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
- Research Center for Precision Environmental Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
| | - Jer-Ming Chang
- Division of Nephrology, Department of Internal Medicine, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan
- Faculty of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan
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Fang T, Zhang Q, Wang Z, Liu JP. Bidirectional association between depression and diabetic nephropathy by meta-analysis. PLoS One 2022; 17:e0278489. [PMID: 36538528 PMCID: PMC9767359 DOI: 10.1371/journal.pone.0278489] [Citation(s) in RCA: 8] [Impact Index Per Article: 2.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/06/2022] [Accepted: 11/16/2022] [Indexed: 12/24/2022] Open
Abstract
BACKGROUND Studies suggested that the association between depression and diabetic nephropathy may be bi-directional, but this hypothesis remains investigating. In this meta-analysis, the bi-directional relationship between depression and diabetic nephropathy was investigated. METHODS A search for the publications on depression and diabetic nephropathy in the databases of PubMed, Web of science, and Embase from the earliest available to August 2022 was conducted. Two sets of pooled risk estimates were calculated using random effects models: diabetic nephropathy predicting depression and depression predicting diabetic nephropathy. Cross-sectional studies were assessed using Agency for Healthcare Research and Quality (AHRQ), cohort and case-control studies were assessed using Newcastle-Ottawa Scale (NOS). RESULT Of the 974,121 patients in 30 clinical studies, 24 studies met eligibility for diabetic nephropathy predicting onset of depression, representing 28,438 incident cases. The other 6 studies met criteria for depression predicting onset of diabetic nephropathy, representing 945,683 incident cases. The pooled odds ratio (OR) of diabetic nephropathy predicting depression was 1.46 (95% CI 1.27-1.67). The OR of depression predicting diabetic nephropathy was 1.22 (95% CI 1.13-1.31). CONCLUSION This meta-analysis shows that the relationship between depression and diabetic nephropathy may be bidirectional. Diabetic nephropathy may be a predictor of depression, and depression may also be an indicator of diabetic nephropathy. The mechanisms underlying the bidirectional relationship need to be further investigated and interventions of the comorbidity of depression and diabetic nephropathy need be studied in clinical practice.
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Affiliation(s)
- Tingting Fang
- Institute of Ageing Research, Hangzhou Normal University, School of Basic Medicine, Hangzhou, Zhejiang Province, China
- School of Public Health, Hangzhou Normal University, Hangzhou, Zhejiang Province, China
- * E-mail: (TF); (JPL)
| | - Qiuling Zhang
- Department of Endocrinology, The Affiliated Hospital of Hangzhou Normal University, Hangzhou, Zhejiang Province, China
| | - Zhiguo Wang
- Institute of Ageing Research, Hangzhou Normal University, School of Basic Medicine, Hangzhou, Zhejiang Province, China
| | - Jun-Ping Liu
- Institute of Ageing Research, Hangzhou Normal University, School of Basic Medicine, Hangzhou, Zhejiang Province, China
- Monash University Department of Immunology and Pathology, Central Clinical School, Faculty of Medicine, Prahran, Victoria, Australia
- Hudson Institute of Medical Research, Clayton, Victoria, Australia
- * E-mail: (TF); (JPL)
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Azhar A, Khan WH, Al-Hosaini K, Zia Q, Kamal MA. Crosstalk between SARS-CoV-2 Infection and Type II Diabetes. Comb Chem High Throughput Screen 2022; 25:2429-2442. [PMID: 35293290 DOI: 10.2174/1386207325666220315114332] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/30/2021] [Revised: 12/11/2021] [Accepted: 12/24/2021] [Indexed: 02/08/2023]
Abstract
Since the outbreak of coronavirus disease (COVID-19) in Wuhan, China, triggered by severe acute respiratory coronavirus 2 (SARS-CoV-2) in late November 2019, spreading to more than 200 countries of the world, the ensuing pandemic to an enormous loss of lives, mainly the older population with comorbidities, like diabetes, cardiovascular disease, chronic obstructive pulmonary disease, obesity, and hypertension. Amongst these immune-debilitating diseases, SARS-CoV-2 infection is the most common in patients with diabetes due to the absence of a normal active immune system to fight the COVID-19. Recovery of patients having a history of diabetes from COVID-19 encounters several complications, and their management becomes cumbersome. For control of coronavirus, antiviral medications, glucose-lowering agents, and steroids have been carefully evaluated. In the present review, we discuss the crosstalk between SARS-CoV-2 infection and patients with a history of diabetes. We mainly emphasize the molecular factors that are involved in diabetic individuals recently infected by SARS-CoV-2 and developed COVID-19 disease. Lastly, we examine the medications available for the long-term management of diabetic patients with SARS-CoV-2 infection.
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Affiliation(s)
- Asim Azhar
- Aligarh College of Education, Aligarh, Uttar Pradesh, India
| | - Wajihul Hasan Khan
- Department of Chemical Engineering, Indian Institute of Technology Delhi, New Delhi, India
| | - Khaled Al-Hosaini
- Department of Pharmacology & Toxicology, College of Pharmacy, King Saud University, Riyadh 11451, Kingdom of Saudi Arabia
| | - Qamar Zia
- Department of Medical Laboratory Sciences, College of Applied Medical Sciences, Majmaah University, Al Majmaah, 11952, Saudi Arabia.,Health and Basic Sciences Research Center, Majmaah University, Al Majmaah 11952, Saudi Arabia
| | - Mohammad Amjad Kamal
- King Fahd Medical Research Center, King Abdulaziz University, Jeddah 21589, Saudi Arabia.,Enzymoics, 7 Peterlee Place, Hebersham, NSW 2770; Novel Global Community Educational Foundation, Australia.,West China School of Nursing / Institutes for Systems Genetics, Frontiers Science Center for Disease- related Molecular Network, West China Hospital, Sichuan University, Chengdu 6141001, Sichuan, China
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