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Haider SA, Sharif R, Sharif F. Multi-Organ Denervation: The Past, Present and Future. J Clin Med 2025; 14:2746. [PMID: 40283576 PMCID: PMC12027612 DOI: 10.3390/jcm14082746] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [Grants] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 02/19/2025] [Revised: 04/04/2025] [Accepted: 04/14/2025] [Indexed: 04/29/2025] Open
Abstract
The sympathetic division of the autonomic nervous system plays a crucial role in maintaining homeostasis, but its overactivity is implicated in various pathological conditions, including hypertension, hyperglycaemia, heart failure, and rheumatoid arthritis. Traditional pharmacotherapies often face limitations such as side effects and poor patient adherence, thus prompting the exploration of device-based multi-organ denervation as a therapeutic strategy. Crucially, this procedure can potentially offer therapeutic benefits throughout the 24 h circadian cycle, described as an "always-on" effect independent of medication compliance and pharmacokinetics. In this comprehensive review, we evaluate the evidence behind targeted multi-organ sympathetic denervation by considering the anatomy and function of the autonomic nervous system, examining the evidence linking sympathetic nervous system overactivity to various cardiometabolic and inflammatory conditions and exploring denervation studies within the literature. So far, renal denervation, developed in 2010, has shown promise in reducing blood pressure and may have broader applications for conditions including arrhythmias, glucose metabolism disorders, heart failure, chronic kidney disease and obstructive sleep apnoea. We review the existing literature surrounding the denervation of other organ systems including the hepatic and splenic arteries, as well as the pulmonary artery and carotid body, which may provide additional physiological benefits and enhance therapeutic effects if carried out simultaneously. Furthermore, we highlight the challenges and future directions for implementing multi-organ sympathetic ablation, emphasising the need for further clinical trials to establish optimal procedural technique, efficacy and safety.
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Affiliation(s)
- Syedah Aleena Haider
- Department of Medicine, University of Galway, H91 TK33 Galway, Ireland
- Department of Cardiology, University Hospital Galway, H91 YR71 Galway, Ireland;
| | - Ruth Sharif
- Department of Cardiology, University Hospital Galway, H91 YR71 Galway, Ireland;
| | - Faisal Sharif
- Department of Medicine, University of Galway, H91 TK33 Galway, Ireland
- Department of Cardiology, University Hospital Galway, H91 YR71 Galway, Ireland;
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Li L, Guo Z, Zhao Y, Liang C, Zheng W, Tian W, Chen Y, Cheng Y, Zhu F, Xiang X. The impact of oxidative stress on abnormal lipid metabolism-mediated disease development. Arch Biochem Biophys 2025; 766:110348. [PMID: 39961502 DOI: 10.1016/j.abb.2025.110348] [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: 11/06/2024] [Revised: 02/09/2025] [Accepted: 02/14/2025] [Indexed: 02/23/2025]
Abstract
Oxidative stress arises from an imbalance between cellular oxidation and anti-oxidation mechanisms, leading to various harmful effects on physiological health. These include inflammatory neutrophil infiltration, increased secretion of proteases, and increased production of oxidative intermediates, all of which significantly contribute to aging and the onset of multiple diseases. This review explores abnormal lipid metabolism, characterized by dysregulation in lipid synthesis, catabolism, digestion, absorption, and transport, with the potential to lead to lipid droplet accumulation or deficit across tissues, thus causing adverse health outcomes. Importantly, the intricate relationship between oxidative stress and inflammation plays a central role in exacerbating metabolic disorders, including diabetes, obesity, hypertension, non-alcoholic fatty liver disease, atherosclerosis, and lung fibrosis. This review seeks to compile and integrate recent research findings on the influence of oxidative stress on abnormal lipid metabolism pathology. A deeper understanding of this connection could reveal new perspectives for advancing the treatment and management of metabolic disorders.
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Affiliation(s)
- Lanlan Li
- Center of Translational Medicine, Zibo Central Hospital, Zibo, 255000, Shandong, China
| | - Zhiliang Guo
- The 80th Group Army Hospital of Chinese PLA, Weifang, Shandong, 261021, China
| | - Yi Zhao
- Shandong Provincial Hospital Affiliated with Shandong's First Medical University, Shandong, China
| | - Chuanjie Liang
- Center of Translational Medicine, Zibo Central Hospital, Zibo, 255000, Shandong, China
| | - Wenxiang Zheng
- Center of Translational Medicine, Zibo Central Hospital, Zibo, 255000, Shandong, China
| | - Wenxiu Tian
- Center of Translational Medicine, Zibo Central Hospital, Zibo, 255000, Shandong, China
| | - Yalin Chen
- Center of Translational Medicine, Zibo Central Hospital, Zibo, 255000, Shandong, China
| | - Yi Cheng
- Center of Translational Medicine, Zibo Central Hospital, Zibo, 255000, Shandong, China
| | - Fengwen Zhu
- Center of Translational Medicine, Zibo Central Hospital, Zibo, 255000, Shandong, China.
| | - Xinxin Xiang
- Center of Translational Medicine, Zibo Central Hospital, Zibo, 255000, Shandong, China.
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Louca P, Berry SE, Bermingham K, Franks PW, Wolf J, Spector TD, Valdes AM, Chowienczyk P, Menni C. Postprandial Responses to a Standardised Meal in Hypertension: The Mediatory Role of Visceral Fat Mass. Nutrients 2022; 14:4499. [PMID: 36364763 PMCID: PMC9655022 DOI: 10.3390/nu14214499] [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: 09/18/2022] [Revised: 10/17/2022] [Accepted: 10/18/2022] [Indexed: 11/16/2022] Open
Abstract
Postprandial insulinaemia, triglyceridaemia and measures of inflammation are thought to be more closely associated with cardiovascular risk than fasting measures. Although hypertension is associated with altered fasting metabolism, it is unknown as to what extent postprandial lipaemic and inflammatory metabolic responses differ between hypertensive and normotensive individuals. Linear models adjusting for age, sex, body mass index (BMI), visceral fat mass (VFM) and multiple testing (false discovery rate), were used to investigate whether hypertensive cases and normotensive controls had different fasting and postprandial (in response to two standardised test meal challenges) lipaemic, glycaemic, insulinaemic, and inflammatory (glycoprotein acetylation (GlycA)) responses in 989 participants from the ZOE PREDICT-1 nutritional intervention study. Compared to normotensive controls, hypertensive individuals had significantly higher fasting and postprandial insulin, triglycerides, and markers of inflammation after adjusting for age, sex, and BMI (effect size: Beta (Standard Error) ranging from 0.17 (0.08), p = 0.04 for peak insulin to 0.29 (0.08), p = 4.4 × 10-4 for peak GlycA). No difference was seen for postprandial glucose. When further adjusting for VFM effects were attenuated. Causal mediation analysis suggests that 36% of the variance in postprandial insulin response and 33.8% of variance in postprandial triglyceride response were mediated by VFM. Hypertensive individuals have different postprandial insulinaemic and lipaemic responses compared to normotensive controls and this is partially mediated by visceral fat mass. Consequently, reducing VFM should be a key focus of health interventions in hypertension. Trial registration: The ClinicalTrials.gov registration identifier is NCT03479866.
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Affiliation(s)
- Panayiotis Louca
- Department of Twin Research, King’s College London, St Thomas’ Hospital Campus, London SE1 7EH, UK
| | - Sarah E. Berry
- Department of Nutritional Sciences, King’s College London, Franklin Wilkins Building, London SE1 9NH, UK
| | - Kate Bermingham
- Department of Twin Research, King’s College London, St Thomas’ Hospital Campus, London SE1 7EH, UK
- Department of Nutritional Sciences, King’s College London, Franklin Wilkins Building, London SE1 9NH, UK
| | - Paul W. Franks
- Genetic & Molecular Epidemiology Unit, Department of Clinical Sciences, Lund University, SE-20502 Malmo, Sweden
| | | | - Tim D. Spector
- Department of Twin Research, King’s College London, St Thomas’ Hospital Campus, London SE1 7EH, UK
| | - Ana M. Valdes
- Nottingham NIHR Biomedical Research Centre, School of Medicine, University of Nottingham, Nottingham NG5 1PB, UK
| | - Phil Chowienczyk
- Vascular Risk & Surgery, King’s College London, St Thomas’ Hospital Campus, London SE1 7EH, UK
| | - Cristina Menni
- Department of Nutritional Sciences, King’s College London, Franklin Wilkins Building, London SE1 9NH, UK
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Refined-JinQi-JiangTang tablet ameliorates hypertension through activation of FGF21/FGFR1 axis in fructose-fed rats. J Nat Med 2022; 76:765-773. [PMID: 35534765 DOI: 10.1007/s11418-022-01626-1] [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: 12/06/2021] [Accepted: 03/20/2022] [Indexed: 10/18/2022]
Abstract
The aim of this study was to investigate the therapeutic effect of JQ-R on metabolic hypertension and its correlation with Fibroblast growth factor 21/Fibroblast growth factor receptors 1(FGF21/FGFR1) pathway. In this study, fructose-induced metabolic hypertension rats were used as hypertension models to detect the regulation effect of JQ-R on hypertension. The effects of JQ-R on blood glucose, blood lipids, serum insulin levels and other metabolic indicators of rats were also measured. The effects of JQ-R on FGF21/FGFR1 signaling pathway in model animals were detected by Real-time quantitative PCR and Western blotting. The results showed that JQ-R significantly reduce the blood pressure of model rats in a dose-dependent manner. Meanwhile, fasting insulin, fasting blood glucose, insulin resistance index, total cholesterol and triglyceride levels were significantly decreased, and glucose and lipid metabolism abnormalities were also significantly improved. JQ-R induces these changes along with FGFR1 phosphorylation, which was also detected in JQ-R treated FGF21 knockout mice. These results suggest that JQ-R can reduce blood pressure and improve glucose and lipid metabolism in fructose-induced hypertension rats. Activation of FGF21/FGFR1 signaling pathway to regulate downstream blood pressure and glucolipid metabolism-related pathways may be one of the important mechanisms of JQ-R in regulating blood pressure.
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Prevalence and risk factors in metabolic syndrome among Temiar in Kelantan. Int J Diabetes Dev Ctries 2021. [DOI: 10.1007/s13410-020-00903-7] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 11/30/2022] Open
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Rodrigues CIS. Biomarker-based Inflammatory Score in Obese Patients with Resistant Hypertension. Arq Bras Cardiol 2019; 112:390-391. [PMID: 30994716 PMCID: PMC6459433 DOI: 10.5935/abc.20190051] [Citation(s) in RCA: 1] [Impact Index Per Article: 0.2] [Reference Citation Analysis] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 11/20/2022] Open
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Catharina AS, Modolo R, Ritter AMV, Sabbatini AR, Lopes HF, Moreno Junior H, Faria APD. Metabolic Syndrome-Related Features in Controlled and Resistant Hypertensive Subjects. Arq Bras Cardiol 2019; 110:514-521. [PMID: 30226908 PMCID: PMC6023630 DOI: 10.5935/abc.20180076] [Citation(s) in RCA: 8] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/03/2017] [Accepted: 12/01/2017] [Indexed: 01/08/2023] Open
Abstract
Background Metabolic syndrome (MetS) is widespread among hypertensive patients. Clinical
features and potential biomarkers of MetS in the presence of hypertension
and resistant hypertension (RHTN) represent a great area of interest for
investigation. Objective The purpose of this study was to evaluate the prevalence of MetS and the
clinical features associated with it in resistant and mild to moderate
hypertensives. Methods This cross-sectional study included 236 patients, (i) 129 mild to moderate
hypertensive patients and (ii) 107 patients with RHTN. We measured blood
pressure (BP) and adipokines levels, and performed bioelectrical impedance
analysis. Microalbuminuria (MA), cardiac hypertrophy and arterial stiffness
were also assessed. The significance level of alpha = 0.05 was adopted. Results We found a MetS prevalence of 73% in resistant and 60% in mild-to-moderate
hypertensive patients. In a multiple regression analysis, MA (odds ratio =
8.51; p = 0.01), leptin/adiponectin ratio (LAR) (odds ratio = 4.13; p =
0.01) and RHTN (odds ratio = 3.75; p = 0.03) were independently associated
with the presence of MetS apart from potential confounders. Conclusions Our findings suggest that both resistant and controlled hypertensive subjects
have a high prevalence of MetS. In addition, MetS-related metabolic
derangements may cause early renal and hormonal changes. Finally, LAR may be
useful as a reliable biomarker for identifying those hypertensive subjects
who are at risk for developing MetS.
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Affiliation(s)
- Arthur Santa Catharina
- Faculdade de Ciências Médicas - Universidade Estadual de Campinas (UNICAMP), Campinas, SP - Brazil
| | - Rodrigo Modolo
- Faculdade de Ciências Médicas - Universidade Estadual de Campinas (UNICAMP), Campinas, SP - Brazil
| | | | | | - Heno Ferreira Lopes
- Instituto do Coração (InCor) - Faculdade de Medicina da Universidade de São Paulo, São Paulo, SP - Brazil
| | - Heitor Moreno Junior
- Faculdade de Ciências Médicas - Universidade Estadual de Campinas (UNICAMP), Campinas, SP - Brazil
| | - Ana Paula de Faria
- Faculdade de Ciências Médicas - Universidade Estadual de Campinas (UNICAMP), Campinas, SP - Brazil
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Cao Q, Yu S, Xiong W, Li Y, Li H, Li J, Li F. Waist-hip ratio as a predictor of myocardial infarction risk: A systematic review and meta-analysis. Medicine (Baltimore) 2018; 97:e11639. [PMID: 30045310 PMCID: PMC6078643 DOI: 10.1097/md.0000000000011639] [Citation(s) in RCA: 41] [Impact Index Per Article: 5.9] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 01/11/2023] Open
Abstract
BACKGROUND AND AIM Several studies have identified that obesity and being overweight can increase the risk of developing myocardial infarction (MI). However, the predictive value of the central obesity index, that is, the waist-hip ratio (WHR), regarding MI risk remains unclear. This study aimed to provide a systematic review and meta-analysis of WHR as a predictor of MI incidence. METHODS This study used relevant keywords and MeSH terms to identify studies of MI risk and WHR from PubMed, Web of Science, Embase, and Cochrane databases in November 2017. RESULTS We conducted a meta-analysis of 12 case-control studies in 14 eligible trials and further explored whether the predictive value of WHR on MI risk varies according to sex. The results showed that a high WHR increased MI risk (pooled odds ratio [OR] 2.62, 95% confidence interval [CI] 2.02-3.39, P < 0.00001) and that elevated WHR is more strongly predictive of MI in women than in men (pooled OR 4.63, 95% CI 3.28-6.53 in women; pooled OR 2.71, 95% CI 2.15-3.41 in men). CONCLUSIONS MI is significantly associated with increased WHR, with a stronger association among women.
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Rogers A, Necola O, Sexias A, Luka A, Newsome V, Williams S, McFarlane SI, Jean-Louis G. Resistant Hypertension and Sleep Duration among Blacks with Metabolic Syndrome MetSO. ACTA ACUST UNITED AC 2016; 5. [PMID: 28066790 DOI: 10.4172/2325-9639.1000183] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/17/2023]
Abstract
INTRODUCTION Resistant hypertension (RHTN) is an important condition affecting 29% of the hypertensive population in the U.S., especially among blacks. Sleep disturbances, like obstructive sleep apnea, insomnia, and short sleep duration, are increasingly recognized as underlying modifiable factors for RHTN. We evaluated associations of RHTN with short sleep duration among blacks with metabolic syndrome. METHODS Data from the Metabolic Syndrome Outcome Study (MetSO), a NIH-funded cohort study characterizing metabolic syndrome (MetS) among blacks were analyzed. MetS was defined according to criteria from the Adult Treatment Panel (ATP III). RHTN was defined according to guidelines from the American Heart Association. Short sleep was defined as self-reported sleep duration <7 hrs experienced during a 24-hour period. RESULTS Analysis was based on 1,035 patients (mean age: 62±14years; female: 69.2%). Of the sample, 90.4% were overweight /obese; 61.4% had diabetes; 74.8% had dyslipidemia; 30.2% had a history of heart disease; and 48% were at high risk for obstructive sleep apnea. Overall, 92.6% reported physician-diagnosed hypertension (HTN) and 20.8% met criteria for RHTN. Analyses showed those with RHTN were more likely to be short sleepers (26.8% vs. 14.9%, p< 0.001). Based on logistic regression analysis, adjusting for effects of age, sex, and medical comorbidities, patients with metabolic syndrome and RHTN had increased odds of being short sleepers (OR = 1.95, 95% CI: 1.28-2.97, p = 0.002). CONCLUSION Among blacks with metabolic syndrome, patients meeting criteria for resistant hypertension showed a twofold greater likelihood of being short sleepers, prompting the need for sleep screening in this vulnerable population.
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Affiliation(s)
- April Rogers
- Center for Healthful Behavior Change (CHBC), Division of Health and Behavior, Department of Population Health, New York University Medical Center, New York, NY 10016, USA
| | - Olivia Necola
- Department of Medicine, Westchester Medical Center, Valhalla, NY 10595, USA
| | - Azizi Sexias
- Center for Healthful Behavior Change (CHBC), Division of Health and Behavior, Department of Population Health, New York University Medical Center, New York, NY 10016, USA
| | - Alla Luka
- Department of Medicine, Division of Endocrinology, State University of New York, Downstate Medical Center, Brooklyn, NY 11203, USA
| | - Valerie Newsome
- Center for Healthful Behavior Change (CHBC), Division of Health and Behavior, Department of Population Health, New York University Medical Center, New York, NY 10016, USA
| | - Stephen Williams
- Center for Healthful Behavior Change (CHBC), Division of Health and Behavior, Department of Population Health, New York University Medical Center, New York, NY 10016, USA
| | - Samy I McFarlane
- Department of Medicine, Division of Endocrinology, State University of New York, Downstate Medical Center, Brooklyn, NY 11203, USA
| | - Girardin Jean-Louis
- Center for Healthful Behavior Change (CHBC), Division of Health and Behavior, Department of Population Health, New York University Medical Center, New York, NY 10016, USA
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Samniang B, Shinlapawittayatorn K, Chunchai T, Pongkan W, Kumfu S, Chattipakorn SC, KenKnight BH, Chattipakorn N. Vagus Nerve Stimulation Improves Cardiac Function by Preventing Mitochondrial Dysfunction in Obese-Insulin Resistant Rats. Sci Rep 2016; 6:19749. [PMID: 26830020 PMCID: PMC4735283 DOI: 10.1038/srep19749] [Citation(s) in RCA: 35] [Impact Index Per Article: 3.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 08/28/2015] [Accepted: 12/17/2015] [Indexed: 01/02/2023] Open
Abstract
Long-term high-fat diet (HFD) consumption leads to not only obese-insulin resistance, but also impaired left ventricular (LV) function. Vagus nerve stimulation (VNS) has been shown to exert cardioprotection. However, its effects on the heart and metabolic parameters under obese-insulin resistant condition is not known. We determined the effects of VNS on metabolic parameters, heart rate variability (HRV) and LV function in obese-insulin resistant rats. Male Wistar rats were fed with HFD for 12 weeks, and were randomly divided into sham and VNS groups. VNS was applied for the next 12 weeks. Echocardiography, blood pressure and HRV were examined. Blood samples were collected for metabolic parameters. At the end, the heart was removed for determination of apoptosis, inflammation, oxidative stress, and cardiac mitochondrial function. VNS for 12 weeks significantly decreased plasma insulin, HOMA index, total cholesterol, triglyceride, LDL and visceral fat. Serum adiponectin was significantly increased in the VNS group. VNS also significantly decreased blood pressure, improved HRV and LV function, decreased cardiac MDA, TNF-α and Bax levels, and improved cardiac mitochondrial function. VNS improves metabolic and hemodynamic parameters, and the LV function via its ability against apoptosis, inflammation and oxidative stress, and preserved cardiac mitochondrial function in obese-insulin resistant rats.
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Affiliation(s)
- Bencharunan Samniang
- Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
- Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
- Center of Excellence in Cardiac Electrophysiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
| | - Krekwit Shinlapawittayatorn
- Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
- Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
- Center of Excellence in Cardiac Electrophysiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
| | - Titikorn Chunchai
- Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
- Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
- Center of Excellence in Cardiac Electrophysiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
| | - Wanpitak Pongkan
- Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
- Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
- Center of Excellence in Cardiac Electrophysiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
| | - Sirinart Kumfu
- Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
- Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
- Center of Excellence in Cardiac Electrophysiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
| | - Siriporn C. Chattipakorn
- Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
- Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
- Center of Excellence in Cardiac Electrophysiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
- Department of Oral Biology and Diagnostic Sciences, Faculty of Dentistry, Chiang Mai University, Chiang Mai, 50200, Thailand
| | | | - Nipon Chattipakorn
- Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
- Cardiac Electrophysiology Unit, Department of Physiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
- Center of Excellence in Cardiac Electrophysiology, Faculty of Medicine, Chiang Mai University, Chiang Mai, 50200, Thailand
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Shuai X, Tao K, Mori M, Kanda T. Bariatric surgery for metabolic syndrome in obesity. Metab Syndr Relat Disord 2015; 13:149-60. [PMID: 25715110 DOI: 10.1089/met.2014.0115] [Citation(s) in RCA: 25] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/16/2022] Open
Abstract
Metabolic syndrome is closely associated with morbid obesity and leads to increased risk of cardiovascular diseases and related mortality. Bariatric surgery is considered an effective option for the management of this condition. We searched MEDLINE, Current Contents, and the Cochrane Library for papers published on bariatric surgery outcomes in English from January 1, 1990, to April 20, 2014. Bariatric surgery can significantly reduce body weight, resolve or cure many of the symptoms of metabolic syndrome, including type 2 diabetes, hypertension, hyperlipidemia, and improve long-term survival. Surgery, in addition to existing therapy, could therefore be considered as an optimal treatment for patients with metabolic syndrome and morbid obesity.
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Affiliation(s)
- Xiaoming Shuai
- 1 Department of Gastrointestinal Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan, Hubei Province, People's Republic of China
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Mulè G, Calcaterra I, Nardi E, Cerasola G, Cottone S. Metabolic syndrome in hypertensive patients: An unholy alliance. World J Cardiol 2014; 6:890-907. [PMID: 25276291 PMCID: PMC4176799 DOI: 10.4330/wjc.v6.i9.890] [Citation(s) in RCA: 45] [Impact Index Per Article: 4.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/29/2014] [Revised: 05/13/2014] [Accepted: 07/18/2014] [Indexed: 02/06/2023] Open
Abstract
For many years, it has been recognized that hypertension tends to cluster with various anthropometric and metabolic abnormalities including abdominal obesity, elevated triglycerides, reduced high-density lipoprotein cholesterol, glucose intolerance, insulin resistance and hyperuricemia. This constellation of various conditions has been transformed from a pathophysiological concept to a clinical entity, which has been defined metabolic syndrome (MetS). The consequences of the MetS have been difficult to assess without commonly accepted criteria to diagnose it. For this reason, on 2009 the International Diabetes Federation, the American Heart Association and other scientific organizations proposed a unified MetS definition. The incidence of the MetS has been increasing worldwide in parallel with an increase in overweight and obesity. The epidemic proportion reached by the MetS represents a major public health challenge, because several lines of evidence showed that the MetS, even without type 2 diabetes, confers an increased risk of cardiovascular morbidity and mortality in different populations including also hypertensive patients. It is likely that the enhanced cardiovascular risk associated with MetS in patients with high blood pressure may be largely mediated through an increased prevalence of preclinical cardiovascular and renal changes, such as left ventricular hypertrophy, early carotid atherosclerosis, impaired aortic elasticity, hypertensive retinopathy and microalbuminuria. Indeed, many reports support this notion, showing that hypertensive patients with MetS exhibit, more often than those without it, these early signs of end organ damage, most of which are recognized as significant independent predictors of adverse cardiovascular outcomes.
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Plasma 8-isoprostane levels are associated with endothelial dysfunction in resistant hypertension. Clin Chim Acta 2014; 433:179-83. [PMID: 24657423 DOI: 10.1016/j.cca.2014.03.009] [Citation(s) in RCA: 27] [Impact Index Per Article: 2.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/29/2013] [Revised: 03/10/2014] [Accepted: 03/11/2014] [Indexed: 02/07/2023]
Abstract
BACKGROUND Impaired endothelial function and arterial stiffness are associated with hypertension and are important risk factors for cardiovascular events. Reactive oxygen species reduce nitric oxide bioavailability and have a pivotal role in endothelial function. Resistant hypertension (RHTN) is characterized by blood pressure (BP) above goal (140/90mmHg) in spite of the concurrent use of ≥3 antihypertensive drugs of different classes. This study evaluated the association between 8-isoprostane levels, an oxidative stress marker, endothelial function and arterial stiffness, in RHTN. METHODS Ninety-four RHTN and 55 well-controlled hypertensive (HT) patients were included. Plasma 8-isoprostane levels were determined by ELISA. Also, flow-mediated dilation (FMD) and pulse wave velocity (PWV) were evaluated to determine endothelial function and arterial stiffness, respectively. RESULTS Levels of 8-isoprostane were markedly higher in RHTN compared to HT patients (22.5±11.2 vs. 17.3±9.8pg/ml, p<0.05, respectively). A significant inverse correlation was observed between FMD and 8-isoprostane (r=-0.35, p=0.001) in RHTN. Finally, multiple logistic regression revealed that 8-isoprostane was a significant predictor of endothelial dysfunction (FMD≤median) in RHTN group. CONCLUSION RHTN showed markedly higher oxidative stress measured by 8-isoprostane, compared to HT patients. Taken together, our findings suggest the involvement of oxidative stress in endothelial function in RHTN.
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Hristova MG. Metabolic syndrome--from the neurotrophic hypothesis to a theory. Med Hypotheses 2013; 81:627-34. [PMID: 23899630 DOI: 10.1016/j.mehy.2013.07.018] [Citation(s) in RCA: 23] [Impact Index Per Article: 1.9] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/03/2013] [Accepted: 07/08/2013] [Indexed: 02/06/2023]
Abstract
Metabolic syndrome (MetS) is a complex and heterogeneous disease characterized by central obesity, impaired glucose metabolism, dyslipidemia, arterial hypertension, insulin resistance and high-sensitivity C-reactive protein. In 2006, a neurotrophic hypothesis of the etiopathogenesis of MetS was launched. This hypothesis considered the neurotrophins a key factor in MetS development. Chronic inflammatory and/or psychoemotional distress provoke a series of neuroimmunoendocrine interactions such as increased tissue and plasma levels of proinflammatory cytokines and neurotrophins, vegetodystonia, disbalance of neurotransmitters, hormones and immunity markers, activation of the hypothalamo-pituitary-adrenal axis, insulin resistance, and atherosclerosis. An early and a late clinical stage in the course of MetS are defined. Meanwhile, evidence of supporting results from the world literature accumulates. This enables the transformation of the definition of the neurotrophic hypothesis into a neurotrophic theory of MetS. The important role of two neurotrophic factors, i.e. the nerve growth factor and brain-derived neurotrophic factor as well as of the proinflammatory cytokines, neurotransmitters, adipokines and, especially, of leptin for the development of MetS, obesity and type 2 diabetes mellitus is illustrated. There are reliable scientific arguments that the metabotrophic deficit due to reduced neurotrophins could be implicated in the pathogenesis of MetS, type 2 diabetes mellitus, and atherosclerosis as well. A special attention is paid to the activity of the hypothalamo-pituitary-adrenal axis after stress. The application of the neurotrophic theory of MetS could contribute to the etiological diagnosis and individualized management of MetS by eliminating the chronic distress, hyponeurotrophinemia and consequent pathology. It helps estimating the risk, defining the prognosis and implementing the effective prevention of this socially significant disease as evidenced by the dramatic recent growth of the world publication output on this interdisciplinary topic.
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Affiliation(s)
- M G Hristova
- Division of Endocrinology, Medical Centre of Varna, Varna, Bulgaria.
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15
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Bryan S, Baregzay B, Spicer D, Singal PK, Khaper N. Redox-inflammatory synergy in the metabolic syndrome. Can J Physiol Pharmacol 2013; 91:22-30. [PMID: 23368637 DOI: 10.1139/cjpp-2012-0295] [Citation(s) in RCA: 51] [Impact Index Per Article: 4.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/15/2022]
Abstract
Metabolic syndrome (MetS) comprises interrelated disease states including obesity, insulin resistance and type 2 diabetes (T2DM), dyslipidemia, and hypertension. Essential to normal physiological function, and yet massively damaging in excess, oxidative stress and inflammation are pivotal common threads among the pathologies of MetS. Increasing evidence indicates that redox and inflammatory dysregulation parallels the syndrome's physiological, biochemical, and anthropometric features, leading many to consider the pro-oxidative, pro-inflammatory milieu an unofficial criterion in itself. Left unchecked, cross-promotion of oxidative stress and inflammation creates a feed-forward cycle that can initiate and advance disease progression. Such redox-inflammatory integration is evident in the pathogenesis of obesity, insulin resistance and T2DM, atherogenic dyslipidemia, and hypertension, and is thus hypothesized to be the "common soil" from which they develop. The present review highlights the synergistic contributions of redox-inflammatory processes to each of the components of the MetS.
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Affiliation(s)
- Sean Bryan
- Medical Sciences Division, Northern Ontario School of Medicine, 955 Oliver Road, Lakehead University, Thunder Bay, ON P7B 5E1, Canada
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16
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Canale MP, Manca di Villahermosa S, Martino G, Rovella V, Noce A, De Lorenzo A, Di Daniele N. Obesity-related metabolic syndrome: mechanisms of sympathetic overactivity. Int J Endocrinol 2013; 2013:865965. [PMID: 24288531 PMCID: PMC3833340 DOI: 10.1155/2013/865965] [Citation(s) in RCA: 142] [Impact Index Per Article: 11.8] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/26/2013] [Accepted: 09/10/2013] [Indexed: 12/15/2022] Open
Abstract
The prevalence of the metabolic syndrome has increased worldwide over the past few years. Sympathetic nervous system overactivity is a key mechanism leading to hypertension in patients with the metabolic syndrome. Sympathetic activation can be triggered by reflex mechanisms as arterial baroreceptor impairment, by metabolic factors as insulin resistance, and by dysregulated adipokine production and secretion from visceral fat with a mainly permissive role of leptin and antagonist role of adiponectin. Chronic sympathetic nervous system overactivity contributes to a further decline of insulin sensitivity and creates a vicious circle that may contribute to the development of hypertension and of the metabolic syndrome and favor cardiovascular and kidney disease. Selective renal denervation is an emerging area of interest in the clinical management of obesity-related hypertension. This review focuses on current understanding of some mechanisms through which sympathetic overactivity may be interlaced to the metabolic syndrome, with particular regard to the role of insulin resistance and of some adipokines.
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Affiliation(s)
- Maria Paola Canale
- Division of Hypertension and Nephrology, Department of System Medicine, University of Rome Tor Vergata, Rome, Italy
| | - Simone Manca di Villahermosa
- Division of Hypertension and Nephrology, Department of System Medicine, University of Rome Tor Vergata, Rome, Italy
| | - Giuliana Martino
- Division of Hypertension and Nephrology, Department of System Medicine, University of Rome Tor Vergata, Rome, Italy
| | - Valentina Rovella
- Division of Hypertension and Nephrology, Department of System Medicine, University of Rome Tor Vergata, Rome, Italy
| | - Annalisa Noce
- Division of Hypertension and Nephrology, Department of System Medicine, University of Rome Tor Vergata, Rome, Italy
| | - Antonino De Lorenzo
- Division of Clinical Nutrition and Nutrigenomic, Department of Biomedicine and Prevention, University of Rome Tor Vergata, Rome, Italy
| | - Nicola Di Daniele
- Division of Hypertension and Nephrology, Department of System Medicine, University of Rome Tor Vergata, Rome, Italy
- *Nicola Di Daniele:
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