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Russell MS, Vasilounis SS, Desroches D, Alenabi T, Drake JDM, Chopp-Hurley JN. Evaluating the Relationship Between Surface and Intramuscular-Based Electromyography Signals: Implications of Subcutaneous Fat Thickness. J Appl Biomech 2025; 41:47-55. [PMID: 39657718 DOI: 10.1123/jab.2024-0101] [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: 04/17/2024] [Revised: 08/06/2024] [Accepted: 09/10/2024] [Indexed: 12/12/2024]
Abstract
Intramuscular (iEMG) and surface electromyographic (sEMG) signals have been compared previously using predictive regression equations, finite element modeling, and correlation and cross-correlation analyses. Although subcutaneous fat thickness (SCFT) has been identified as a primary source of sEMG signal amplitude attenuation and low-pass filter equivalence, few studies have explored the potential effect of SCFT on sEMG and iEMG signal characteristics. The purpose of this study was to investigate the relationship between normalized submaximal iEMG and sEMG signal amplitudes collected from 4 muscles (rectus femoris, vastus lateralis, infraspinatus, and erector spinae) and determine whether SCFT explains more variance in this relationship. The effect of sex was also explored. Linear regression models demonstrated that the relationship between sEMG and iEMG was highly variable across the muscles examined (adjusted coefficient of determination [Adj R2] = .02-.74). SCFT improved the model fit for vastus lateralis, although this relationship only emerged with the inclusion of sex as a covariate. Thus, this research suggests that SCFT is not a prominent factor affecting the linearity between sEMG and iEMG. Researchers should investigate other parameters that may affect the linearity between sEMG and iEMG signals.
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Affiliation(s)
- Matthew S Russell
- School of Kinesiology and Health Science, York University, Toronto, ON, Canada
| | - Sam S Vasilounis
- School of Kinesiology and Health Science, York University, Toronto, ON, Canada
| | - Daniel Desroches
- School of Kinesiology and Health Science, York University, Toronto, ON, Canada
| | - Talia Alenabi
- Department of Kinesiology, University of Waterloo, Waterloo, ON, Canada
| | - Janessa D M Drake
- School of Kinesiology and Health Science, York University, Toronto, ON, Canada
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2
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Guglielmi V, Dalle Grave R, Leonetti F, Solini A. Female obesity: clinical and psychological assessment toward the best treatment. Front Endocrinol (Lausanne) 2024; 15:1349794. [PMID: 38765954 PMCID: PMC11099266 DOI: 10.3389/fendo.2024.1349794] [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: 12/05/2023] [Accepted: 04/19/2024] [Indexed: 05/22/2024] Open
Abstract
Obesity is a heterogeneous condition which results from complex interactions among sex/gender, sociocultural, environmental, and biological factors. Obesity is more prevalent in women in most developed countries, and several clinical and psychological obesity complications show sex-specific patterns. Females differ regarding fat distribution, with males tending to store more visceral fat, which is highly correlated to increased cardiovascular risk. Although women are more likely to be diagnosed with obesity and appear more motivated to lose weight, as confirmed by their greater representation in clinical trials, males show better outcomes in terms of body weight and intra-abdominal fat loss and improvements in the metabolic risk profile. However, only a few relatively recent studies have investigated gender differences in obesity, and sex/gender is rarely considered in the assessment and management of the disease. This review summarizes the evidence of gender differences in obesity prevalence, contributing factors, clinical complications, and psychological challenges. In addition, we explored gender differences in response to obesity treatments in the specific context of new anti-obesity drugs.
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Affiliation(s)
- Valeria Guglielmi
- Unit of Internal Medicine and Obesity Center, Department of Systems Medicine, Policlinico Tor Vergata, University of Rome Tor Vergata, Rome, Italy
| | - Riccardo Dalle Grave
- Department of Eating and Weight Disorders, Villa Garda Hospital, Garda, VR, Italy
| | - Frida Leonetti
- Department of Medical-Surgical Sciences and Biotechnologies, Sapienza University of Rome, Rome, Italy
| | - Anna Solini
- Department of Surgical, Medical, Molecular and Critical Area Pathology, University of Pisa, Pisa, Italy
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Babic A, Wang QL, Lee AA, Yuan C, Rifai N, Luo J, Tabung FK, Shadyab AH, Wactawski-Wende J, Saquib N, Kim J, Kraft P, Sesso HD, Buring JE, Giovannucci EL, Manson JE, Stampfer MJ, Ng K, Fuchs CS, Wolpin BM. Sex-Specific Associations between Adiponectin and Leptin Signaling and Pancreatic Cancer Survival. Cancer Epidemiol Biomarkers Prev 2023; 32:1458-1469. [PMID: 37555827 PMCID: PMC10592159 DOI: 10.1158/1055-9965.epi-23-0505] [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: 05/04/2023] [Revised: 07/17/2023] [Accepted: 08/07/2023] [Indexed: 08/10/2023] Open
Abstract
BACKGROUND Circulating adiponectin and leptin have been associated with risk of pancreatic cancer. However, the relationship between long-term exposure to these adipokines in the prediagnostic period with patient survival has not been investigated. METHODS Adipokine levels were measured in prospectively collected samples from 472 patients with pancreatic cancer. Because of sex-specific differences in adipokine levels, associations were evaluated separately for men and women. In a subset of 415 patients, we genotyped 23 SNPs in adiponectin receptor genes (ADIPOR1 and ADIPOR2) and 30 SNPs in the leptin receptor gene (LEPR). RESULTS Adiponectin levels were inversely associated with survival in women [HR, 1.71; 95% confidence interval (CI), 1.15-2.54]; comparing top with bottom quartile but not in men (HR, 0.89; 95% CI, 0.46-1.70). The SNPs rs10753929 and rs1418445 in ADIPOR1 were associated with survival in the combined population (per minor allele HR, 0.66; 95% CI, 0.51-0.84, and HR, 1.33; 95% CI, 1.12-1.58, respectively). Among SNPs in LEPR, rs12025906, rs3790431, and rs17127601 were associated with survival in the combined population [HRs, 1.54 (95% CI, 1.25-1.90), 0.72 (95% CI, 0.59-0.88), and 0.70 (95% CI, 0.56-0.89), respectively], whereas rs11585329 was associated with survival in men only (HR, 0.39; 95% CI, 0.23-0.66; Pinteraction = 0.0002). CONCLUSIONS High levels of adiponectin in the prediagnostic period were associated with shorter survival among women, but not among men with pancreatic cancer. Several polymorphisms in ADIPOR1 and LEPR are associated with patient survival. IMPACT Our findings reveal the association between adipokine signaling and pancreatic cancer survival and demonstrate the importance of examining obesity-associated pathways in relation to pancreatic cancer in a sex-specific manner.
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Affiliation(s)
- Ana Babic
- Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA
| | - Qiao-Li Wang
- Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA
| | - Alice A. Lee
- Division of Gastroenterology, Hepatology, and Endoscopy, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA
| | - Chen Yuan
- Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA
| | - Nader Rifai
- Department of Laboratory Medicine, Children’s Hospital Boston, Boston, MA
| | - Juhua Luo
- Department of Epidemiology and Biostatistics, School of Public Health, Indiana University, Bloomington, IN
| | - Fred K. Tabung
- Department of Internal Medicine, Ohio State University, Columbus, OH
- Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA
| | - Aladdin H. Shadyab
- Herbert Wertheim School of Public Health and Human Longevity Science, University of California, San Diego, La Jolla, CA
| | - Jean Wactawski-Wende
- Department of Epidemiology and Environmental Health, School of Public Health and Health Professions, State University of New York, Buffalo, NY
| | - Nazmus Saquib
- College of Medicine, Sulaiman Al Rajhi University, Al Bukairiyah, Kingdom of Saudi Arabia
| | - Jihye Kim
- Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA
| | - Peter Kraft
- Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA
- Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, MA
| | - Howard D. Sesso
- Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA
- Division of Preventive Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA
| | - Julie E. Buring
- Division of Preventive Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA
- Department of Ambulatory Care and Prevention, Harvard Medical School, Boston, MA
| | - Edward L. Giovannucci
- Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA
- Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital, and Harvard Medical School, Boston, MA
| | - JoAnn E. Manson
- Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA
- Division of Preventive Medicine, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital, and Harvard Medical School, Boston, MA
| | - Meir J. Stampfer
- Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, MA
- Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, MA
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women’s Hospital, and Harvard Medical School, Boston, MA
| | - Kimmie Ng
- Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA
| | - Charles S. Fuchs
- Hematology and Oncology Product Development, Genentech & Roche, South San Francisco, CA
| | - Brian M. Wolpin
- Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA
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Hu Y, Liu L, Chen Y, Zhang X, Zhou H, Hu S, Li X, Li M, Li J, Cheng S, Liu Y, Xu Y, Yan W. Cancer-cell-secreted miR-204-5p induces leptin signalling pathway in white adipose tissue to promote cancer-associated cachexia. Nat Commun 2023; 14:5179. [PMID: 37620316 PMCID: PMC10449837 DOI: 10.1038/s41467-023-40571-9] [Citation(s) in RCA: 28] [Impact Index Per Article: 14.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/31/2023] [Accepted: 08/01/2023] [Indexed: 08/26/2023] Open
Abstract
Cancer-associated cachexia is a multi-organ weight loss syndrome, especially with a wasting disorder of adipose tissue and skeletal muscle. Small extracellular vesicles (sEVs) serve as emerging messengers to connect primary tumour and metabolic organs to exert systemic regulation. However, whether and how tumour-derived sEVs regulate white adipose tissue (WAT) browning and fat loss is poorly defined. Here, we report breast cancer cell-secreted exosomal miR-204-5p induces hypoxia-inducible factor 1A (HIF1A) in WAT by targeting von Hippel-Lindau (VHL) gene. Elevated HIF1A protein induces the leptin signalling pathway and thereby enhances lipolysis in WAT. Additionally, exogenous VHL expression blocks the effect of exosomal miR-204-5p on WAT browning. Reduced plasma phosphatidyl ethanolamine level is detected in mice lack of cancer-derived miR-204-5p secretion in vivo. Collectively, our study reveals circulating miR-204-5p induces hypoxia-mediated leptin signalling pathway to promote lipolysis and WAT browning, shedding light on both preventive screenings and early intervention for cancer-associated cachexia.
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Affiliation(s)
- Yong Hu
- Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China
- Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 430062, China
| | - Liu Liu
- Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China
| | - Yong Chen
- Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China
| | - Xiaohui Zhang
- Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China
| | - Haifeng Zhou
- Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China
| | - Sheng Hu
- Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China
| | - Xu Li
- Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China
| | - Meixin Li
- Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China
| | - Juanjuan Li
- Department of Breast and Thyroid Surgery, Renmin Hospital of Wuhan University, Wuhan, Hubei, 430060, China
| | - Siyuan Cheng
- Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 430062, China
| | - Yong Liu
- Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China
- Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences; TaiKang Center for Life and Medical Sciences; The Institute for Advanced Studies; Frontier Science Center for Immunology and Metabolism, Wuhan University, Wuhan, Hubei, 430072, China
| | - Yancheng Xu
- Department of Endocrinology, Zhongnan Hospital of Wuhan University, Wuhan, Hubei, 430062, China.
| | - Wei Yan
- Hubei Key Laboratory of Cell Homeostasis, College of Life Sciences, TaiKang Center for Life and Medical Sciences, Zhongnan Hospital of Wuhan University, Wuhan University, Wuhan, Hubei, 430072, China.
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Gu P, Ding K, Lu L, Zhang Y, Wang W, Guo Q, Liao Y, Yang B, Wang T, Zhou C, Lu B, Kong APS, Cheng AS, Hui HX, Shao J. Compromised browning in white adipose tissue of ageing people. Eur J Endocrinol 2023; 188:lvad014. [PMID: 36750512 DOI: 10.1093/ejendo/lvad014] [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: 09/27/2022] [Revised: 11/18/2022] [Accepted: 02/03/2023] [Indexed: 02/09/2023]
Abstract
BACKGROUND Adipose tissue plays a pivotal role in the pathology of metabolic disorders. In the past decade, brown and brown-like adipose tissues were detected in adult humans and show therapeutic potential in ageing-related metabolic diseases. OBJECTIVE This study investigated expressions of major brown adipose markers in white adipose tissue (WAT) of different ages. Their associations with metabolic parameters and key adipokines were interrogated. DESIGN Cross-sectional study, 2019-2021. METHODS We recruited 21 young, 67 middle-aged, and 34 older patients. Omental adipose tissues were collected, and expressions of key brown markers and adipokines and the adipocyte size were evaluated. The fat depot distribution was evaluated by computed tomography. RESULTS UCP1 and PRDM16 mRNA expressions declined with ageing in WAT and were more associated with age, than with the body mass index (BMI). The increased visceral adipose tissue (VAT) amount, as well as the VAT to subcutaneous adipose tissue (SAT) ratio, was decreased in the highest tertile of UCP1 expression, while individuals in different PRDM16 mRNA tertiles exhibited similar fat distribution. UCP1 mRNA was positively correlated with ADIPOQ and the strength of the correlation declined with ageing. In contrast, the association between UCP1 and LEP was insignificant in young and middle-aged groups but became significantly correlated in the older-people group. We also found a positive correlation between UCP1 and PRDM16. CONCLUSIONS PRDM16 and UCP1, despite their key functions in adipose browning, exhibit differential clinical correlations with metabolic features in human WAT in an age-dependent manner. These two genes may participate in the pathogenesis of ageing-related metabolic diseases, but with distinct mechanisms.
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Affiliation(s)
- Ping Gu
- Department of Endocrinology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 210000, China
| | - Kai Ding
- Research Institute of General Surgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 210000, China
| | - Lei Lu
- Department of Endocrinology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 210000, China
| | - Yu Zhang
- Department of Anesthesiology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 210000, China
| | - Wei Wang
- Department of Endocrinology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 210000, China
| | - Qingyu Guo
- Department of Endocrinology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 210000, China
| | - Yannian Liao
- Research Institute of General Surgery, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 210000, China
| | - Bingjie Yang
- Department of Endocrinology, Jinling Hospital, Nanjing Med University, Nanjing 210000, China
| | - Tiantian Wang
- Department of Endocrinology, Jinling Hospital, Nanjing Med University, Nanjing 210000, China
| | - Changsheng Zhou
- Department of Medical Imaging, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 210000, China
| | - Bin Lu
- Department of Endocrinology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 210000, China
| | - Alice P S Kong
- Department of Medicine and Therapeutics, Hong Kong Special Administrative Region, The Chinese University of Hong Kong, Hong Kong, China
- Hong Kong Institute of Diabetes and Obesity, The Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong Special Administrative Region, Shatin, Hong Kong, China
- Li Ka Shing Institute of Health Sciences, The Chinese University of Hong Kong, Prince of Wales Hospital, Hong Kong Special Administrative Region, Shatin, Hong Kong, China
| | - Alfred S Cheng
- School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China
| | - Hannah Xiaoyan Hui
- School of Biomedical Sciences, The Chinese University of Hong Kong, Hong Kong, China
| | - Jiaqing Shao
- Department of Endocrinology, Jinling Hospital, School of Medicine, Nanjing University, Nanjing 210000, China
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Zenno A, Brady SM, Faulkner LM, Ballenger KL, Fatima S, Yanovski JA. Circadian variation of serum leptin and adipose tissue changes in children. Pediatr Obes 2023; 18:e12984. [PMID: 36161713 PMCID: PMC9851946 DOI: 10.1111/ijpo.12984] [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: 04/05/2022] [Revised: 07/25/2022] [Accepted: 09/12/2022] [Indexed: 02/06/2023]
Abstract
BACKGROUND Higher morning serum leptin values are associated with larger adipose tissue gains in children; however, it is unclear if leptin circadian variation is itself associated with adipose tissue changes during growth. OBJECTIVE We studied the association of circadian variation in leptin with change in total body fat mass (TBFM), total body percentage fat (%FM), and trunk fat mass (TrFM). METHODS Baseline serum samples for leptin were obtained every 3 h for 24 h from 130 children (baseline age 9.6 ± 2.5y; 51.1% male; BMI-Z 1.59) with mean follow-up of 11.1 ± 4.0y and underwent dual-energy x-ray absorptiometry. ANCOVA models examined change in TBFM, %FM, or TrFM as dependent variables and number of years of follow-up, sex, race, baseline age, pubertal status, initial visit body composition, and initial visit serum leptin circadian variables (maximal diurnal leptin [acrophase], diurnal amplitude, and percentage change of amplitude) as independent factors. RESULT Although initial visit mesor (24 h average) leptin was positively associated with initial visit TBFM (r2 = 0.78, p < 0.001), %FM (r2 = 076, p < 0.001), and TrFM (r2 = 0.71, p < 0.001), none of the circadian leptin variables studied was significantly associated with change in TBFM, %FM, or TrFM. CONCLUSION We found no evidence that circadian variation in serum leptin concentrations during childhood is associated with long-term changes in children's adiposity.
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Affiliation(s)
- Anna Zenno
- Section on Growth and Obesity (SGO), Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), DHHS, Bethesda, Maryland, USA
| | - Sheila M Brady
- Section on Growth and Obesity (SGO), Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), DHHS, Bethesda, Maryland, USA
| | - Loie M Faulkner
- Section on Growth and Obesity (SGO), Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), DHHS, Bethesda, Maryland, USA
| | - Kaitlin L Ballenger
- Section on Growth and Obesity (SGO), Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), DHHS, Bethesda, Maryland, USA
| | - Syeda Fatima
- Section on Growth and Obesity (SGO), Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), DHHS, Bethesda, Maryland, USA
| | - Jack A Yanovski
- Section on Growth and Obesity (SGO), Division of Intramural Research, Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD), National Institutes of Health (NIH), DHHS, Bethesda, Maryland, USA
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Lederer AK, Storz MA, Huber R, Hannibal L, Neumann E. Plasma Leptin and Adiponectin after a 4-Week Vegan Diet: A Randomized-Controlled Pilot Trial in Healthy Participants. INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH 2022; 19:ijerph191811370. [PMID: 36141644 PMCID: PMC9517500 DOI: 10.3390/ijerph191811370] [Citation(s) in RCA: 0] [Impact Index Per Article: 0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Subscribe] [Scholar Register] [Received: 08/08/2022] [Revised: 09/05/2022] [Accepted: 09/06/2022] [Indexed: 05/12/2023]
Abstract
Adiponectin and leptin are important mediators of metabolic homeostasis. The actions of these adipokines extend beyond adipocytes and include systemic modulation of lipid and glucose metabolism, nutrient flux, and the immune response to changes in nutrition. Herein, we hypothesized that short-term intervention with a vegan diet might result in an improvement of plasma concentrations of adiponectin and leptin and the leptin/adiponectin ratio. We investigated the response of plasma adiponectin and leptin to a 4-week intervention with a vegan or meat-rich diet and its associations with sex, BMI and nutritional intake. Fifty-three healthy, omnivore participants (62% female, average age 31 years and BMI 23.1 kg/m2) were randomly assigned to a vegan or meat-rich diet for 4 weeks. Plasma adiponectin and leptin were lower in men compared to women both at the beginning and end of the trial. The concentration of adiponectin in women was significantly higher both when comparing their transition from omnivorous to vegan diet (p = 0.023) and also for vegan versus meat-rich diet at the end of the trial (p = 0.001), whereas plasma leptin did not vary significantly. No changes in adiponectin were identified in men, yet an increase in leptin occurred upon their transition from an omnivorous to a meat-rich diet (p = 0.019). Examination of plasma adiponectin/leptin ratio, a proposed marker of cardiovascular risk, did not differ after 4-weeks of dietary intervention. Our study revealed that adiponectin and leptin concentrations are sensitive to short-term dietary intervention in a sex-dependent manner. This dietary modification of leptin and adiponectin not only occurs quickly as demonstrated in our study, but it remains such as published in studies with individuals who are established (long-term) vegetarians compared to omnivorous.
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Affiliation(s)
- Ann-Kathrin Lederer
- Center for Complementary Medicine, Department of Medicine II, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany
- Department of General, Visceral, and Transplant Surgery, University Medical Center Mainz, 55131 Mainz, Germany
- Correspondence: ; Tel.: +49-761-27082010
| | - Maximilian Andreas Storz
- Center for Complementary Medicine, Department of Medicine II, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany
| | - Roman Huber
- Center for Complementary Medicine, Department of Medicine II, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany
| | - Luciana Hannibal
- Laboratory of Clinical Biochemistry and Metabolism, Department of General Pediatrics, Adolescent Medicine and Neonatology, Medical Center-University of Freiburg, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany
| | - Elena Neumann
- Department of Rheumatology and Clinical Immunology, Campus Kerckhoff, Justus-Liebig-University Giessen, 61213 Bad Nauheim, Germany
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8
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Haque N, Tischkau SA. Sexual Dimorphism in Adipose-Hypothalamic Crosstalk and the Contribution of Aryl Hydrocarbon Receptor to Regulate Energy Homeostasis. Int J Mol Sci 2022; 23:ijms23147679. [PMID: 35887027 PMCID: PMC9322714 DOI: 10.3390/ijms23147679] [Citation(s) in RCA: 2] [Impact Index Per Article: 0.7] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/16/2022] [Revised: 07/08/2022] [Accepted: 07/09/2022] [Indexed: 11/16/2022] Open
Abstract
There are fundamental sex differences in the regulation of energy homeostasis. Better understanding of the underlying mechanisms of energy balance that account for this asymmetry will assist in developing sex-specific therapies for sexually dimorphic diseases such as obesity. Multiple organs, including the hypothalamus and adipose tissue, play vital roles in the regulation of energy homeostasis, which are regulated differently in males and females. Various neuronal populations, particularly within the hypothalamus, such as arcuate nucleus (ARC), can sense nutrient content of the body by the help of peripheral hormones such leptin, derived from adipocytes, to regulate energy homeostasis. This review summarizes how adipose tissue crosstalk with homeostatic network control systems in the brain, which includes energy regulatory regions and the hypothalamic–pituitary axis, contribute to energy regulation in a sex-specific manner. Moreover, development of obesity is contingent upon diet and environmental factors. Substances from diet and environmental contaminants can exert insidious effects on energy metabolism, acting peripherally through the aryl hydrocarbon receptor (AhR). Developmental AhR activation can impart permanent alterations of neuronal development that can manifest a number of sex-specific physiological changes, which sometimes become evident only in adulthood. AhR is currently being investigated as a potential target for treating obesity. The consensus is that impaired function of the receptor protects from obesity in mice. AhR also modulates sex steroid receptors, and hence, one of the objectives of this review is to explain why investigating sex differences while examining this receptor is crucial. Overall, this review summarizes sex differences in the regulation of energy homeostasis imparted by the adipose–hypothalamic axis and examines how this axis can be affected by xenobiotics that signal through AhR.
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Affiliation(s)
- Nazmul Haque
- Department of Pharmacology, Southern Illinois University School of Medicine, Springfield, IL 62702, USA;
| | - Shelley A. Tischkau
- Department of Pharmacology, Southern Illinois University School of Medicine, Springfield, IL 62702, USA;
- Department of Medical Microbiology, Immunology and Cell Biology, Southern Illinois University School of Medicine, Springfield, IL 62702, USA
- Correspondence:
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9
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Mank JE, Rideout EJ. Developmental mechanisms of sex differences: from cells to organisms. Development 2021; 148:272484. [PMID: 34647574 DOI: 10.1242/dev.199750] [Citation(s) in RCA: 22] [Impact Index Per Article: 5.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 01/10/2023]
Abstract
Male-female differences in many developmental mechanisms lead to the formation of two morphologically and physiologically distinct sexes. Although this is expected for traits with prominent differences between the sexes, such as the gonads, sex-specific processes also contribute to traits without obvious male-female differences, such as the intestine. Here, we review sex differences in developmental mechanisms that operate at several levels of biological complexity - molecular, cellular, organ and organismal - and discuss how these differences influence organ formation, function and whole-body physiology. Together, the examples we highlight show that one simple way to gain a more accurate and comprehensive understanding of animal development is to include both sexes.
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Affiliation(s)
- Judith E Mank
- Department of Zoology, Biodiversity Research Centre, The University of British Columbia, Vancouver, BC V6T 1Z4, Canada.,Biosciences, University of Exeter, Penryn Campus, Penryn TR10 9FE, UK
| | - Elizabeth J Rideout
- Department of Cellular and Physiological Sciences, Life Sciences Institute, The University of British Columbia, Vancouver, BC V6T 1Z3, Canada
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10
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Šimják P, Anderlová K, Cinkajzlová A, Pařízek A, Kršek M, Haluzík M. The possible role of endocrine dysfunction of adipose tissue in gestational diabetes mellitus. MINERVA ENDOCRINOL 2021; 45:228-242. [PMID: 33000620 DOI: 10.23736/s0391-1977.20.03192-2] [Citation(s) in RCA: 6] [Impact Index Per Article: 1.5] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
Gestational diabetes mellitus (GDM) is diabetes that is first diagnosed in the second or third trimester of pregnancy in patients who did not have a history of diabetes before pregnancy. Consequences of GDM include increased risk of macrosomia and birth complications in the infant and an increased risk of maternal type 2 diabetes mellitus (T2DM) after pregnancy. There is also a longer-term risk of obesity, T2DM, and cardiovascular diseases in the child. GDM is the result of impaired glucose tolerance due to pancreatic β-cell dysfunction on a background of insulin resistance that physiologically increases during pregnancy. The strongest clinical predictors of GDM are overweight and obesity. The fact that women with GDM are more likely to be overweight or obese suggests that adipose tissue dysfunction may be involved in the pathogenesis of GDM, similarly to T2DM. Adipose tissue is not only involved in energy storage but also functions as an active endocrine organ secreting adipokines (specific hormones and cytokines) with the ability to alter insulin sensitivity. Recent evidence points to a crucial role of numerous adipokines produced by fat in the development of GDM. The following text summarizes the current knowledge about a possible role of selected adipokines in the development of GDM.
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Affiliation(s)
- Patrik Šimják
- Department of Gynecology and Obstetrics, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic
| | - Kateřina Anderlová
- Department of Gynecology and Obstetrics, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic.,Third Department of Medicine, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic
| | - Anna Cinkajzlová
- Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic
| | - Antonín Pařízek
- Department of Gynecology and Obstetrics, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic
| | - Michal Kršek
- Third Department of Medicine, First Faculty of Medicine, Charles University and General University Hospital, Prague, Czech Republic
| | - Martin Haluzík
- Diabetes Center, Institute for Clinical and Experimental Medicine, Prague, Czech Republic -
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11
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Zhang L, Clark T, Gopalasingam G, Neely GG, Herzog H. Ninjin'yoeito modulates feeding and activity under negative energy balance conditions via the NPY system. Neuropeptides 2021; 87:102149. [PMID: 33882337 DOI: 10.1016/j.npep.2021.102149] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 10/12/2020] [Revised: 01/17/2021] [Accepted: 03/03/2021] [Indexed: 12/17/2022]
Abstract
The central and peripheral neuropeptide Y (NPY) system is critically involved in feeding and energy homeostasis control. Disease conditions as well as aging can lead to reduced functionality of the NPY system and boosting it represents a promising option to improve health outcomes in these situations. Here we show that Ninjin-yoeito (NYT), a Japanese kampo medicine comprising twelve herbs, and known to be effective to treat anorexia and frailty, mediates part of its action via NPY/peptide YY (PYY) related pathways. Especially under negative energy homeostasis conditions NYT is able to promote feeding and reduces activity to conserve energy. These effects are in part mediated via signalling through the NPY system since lack of Y4 receptors or PYY leading to modification in these responses highlighting the possibility for combination treatment to improve aging related conditions on energy homeostasis control.
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Affiliation(s)
- Lei Zhang
- Neuroscience Division, Garvan Institute of Medical Research, St Vincent's Hospital, Darlinghurst, Sydney, Australia; St. Vincent's Clinical School, University of NSW, Sydney, Australia.
| | - Tereli Clark
- The Charles Perkins Centre, School of Life & Environmental Sciences, The University of Sydney, NSW 2006, Australia
| | - Gopana Gopalasingam
- Neuroscience Division, Garvan Institute of Medical Research, St Vincent's Hospital, Darlinghurst, Sydney, Australia
| | - G Gregory Neely
- The Charles Perkins Centre, School of Life & Environmental Sciences, The University of Sydney, NSW 2006, Australia
| | - Herbert Herzog
- Neuroscience Division, Garvan Institute of Medical Research, St Vincent's Hospital, Darlinghurst, Sydney, Australia; School of Medical Sciences, University of NSW, Sydney, NSW, Australia; Faculty of Medicine, University of NSW, Sydney, NSW, Australia
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12
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Al-Mrabeh A. β-Cell Dysfunction, Hepatic Lipid Metabolism, and Cardiovascular Health in Type 2 Diabetes: New Directions of Research and Novel Therapeutic Strategies. Biomedicines 2021; 9:226. [PMID: 33672162 PMCID: PMC7927138 DOI: 10.3390/biomedicines9020226] [Citation(s) in RCA: 14] [Impact Index Per Article: 3.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/31/2020] [Revised: 02/09/2021] [Accepted: 02/17/2021] [Indexed: 02/06/2023] Open
Abstract
Cardiovascular disease (CVD) remains a major problem for people with type 2 diabetes mellitus (T2DM), and dyslipidemia is one of the main drivers for both metabolic diseases. In this review, the major pathophysiological and molecular mechanisms of β-cell dysfunction and recovery in T2DM are discussed in the context of abnormal hepatic lipid metabolism and cardiovascular health. (i) In normal health, continuous exposure of the pancreas to nutrient stimulus increases the demand on β-cells. In the long term, this will not only stress β-cells and decrease their insulin secretory capacity, but also will blunt the cellular response to insulin. (ii) At the pre-diabetes stage, β-cells compensate for insulin resistance through hypersecretion of insulin. This increases the metabolic burden on the stressed β-cells and changes hepatic lipoprotein metabolism and adipose tissue function. (iii) If this lipotoxic hyperinsulinemic environment is not removed, β-cells start to lose function, and CVD risk rises due to lower lipoprotein clearance. (iv) Once developed, T2DM can be reversed by weight loss, a process described recently as remission. However, the precise mechanism(s) by which calorie restriction causes normalization of lipoprotein metabolism and restores β-cell function are not fully established. Understanding the pathophysiological and molecular basis of β-cell failure and recovery during remission is critical to reduce β-cell burden and loss of function. The aim of this review is to highlight the link between lipoprotein export and lipid-driven β-cell dysfunction in T2DM and how this is related to cardiovascular health. A second aim is to understand the mechanisms of β-cell recovery after weight loss, and to explore new areas of research for developing more targeted future therapies to prevent T2DM and the associated CVD events.
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Affiliation(s)
- Ahmad Al-Mrabeh
- Faculty of Medical Sciences, Translational and Clinical Research Institute, Magnetic Resonance Centre, Newcastle University, Newcastle upon Tyne NE2 4HH, UK
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13
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Physical activity and cancer risk. Actual knowledge and possible biological mechanisms. Radiol Oncol 2021; 55:7-17. [PMID: 33885236 PMCID: PMC7877262 DOI: 10.2478/raon-2020-0063] [Citation(s) in RCA: 32] [Impact Index Per Article: 8.0] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/11/2020] [Accepted: 09/25/2020] [Indexed: 02/07/2023] Open
Abstract
Background Scientific evidence has shown that an increase in regular physical activity is associated with a decrease in the development of many types of cancer. Potential mechanisms that link physical activity to reduced cancer risk include a decrease in systemic inflammation, hyperinsulinemia, insulin-like growth factor (IGF-I), sex hormones, pro-inflammatory leptin and other obesity-related cytokines, and a significant increase in anti-inflammatory adiponectin levels. In addition, physical activity improves immune function and the composition and diversity of the gastrointestinal microbiota. Moderate physical activity is important for cancer protection, but the most significant changes in the inflammatory profile are conferred by physical activity performed at higher intensities. Thus, there is a need for further investigation into the type, intensity, and duration of physical activity for the prevention of some types of cancer and the development of effective recommendations. Conclusions There is a strong evidence that physical activity of moderate to vigorous intensity protects against colon and breast cancer, and probably against cancer at all other sites.
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14
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Goossens GH, Jocken JWE, Blaak EE. Sexual dimorphism in cardiometabolic health: the role of adipose tissue, muscle and liver. Nat Rev Endocrinol 2021; 17:47-66. [PMID: 33173188 DOI: 10.1038/s41574-020-00431-8] [Citation(s) in RCA: 195] [Impact Index Per Article: 48.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Accepted: 10/02/2020] [Indexed: 12/11/2022]
Abstract
Obesity is associated with many adverse health effects, such as an increased cardiometabolic risk. Despite higher adiposity for a given BMI, premenopausal women are at lower risk of cardiometabolic disease than men of the same age. This cardiometabolic advantage in women seems to disappear after the menopause or when type 2 diabetes mellitus develops. Sexual dimorphism in substrate supply and utilization, deposition of excess lipids and mobilization of stored lipids in various key metabolic organs (such as adipose tissue, skeletal muscle and the liver) are associated with differences in tissue-specific insulin sensitivity and cardiometabolic risk profiles between men and women. Moreover, lifestyle-related factors and epigenetic and genetic mechanisms seem to affect metabolic complications and disease risk in a sex-specific manner. This Review provides insight into sexual dimorphism in adipose tissue distribution, adipose tissue, skeletal muscle and liver substrate metabolism and tissue-specific insulin sensitivity in humans, as well as the underlying mechanisms, and addresses the effect of these sex differences on cardiometabolic health. Additionally, this Review highlights the implications of sexual dimorphism in the pathophysiology of obesity-related cardiometabolic risk for the development of sex-specific prevention and treatment strategies.
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Affiliation(s)
- Gijs H Goossens
- Department of Human Biology, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Centre+, Maastricht, Netherlands.
| | - Johan W E Jocken
- Department of Human Biology, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Centre+, Maastricht, Netherlands
| | - Ellen E Blaak
- Department of Human Biology, NUTRIM School of Nutrition and Translational Research in Metabolism, Maastricht University Medical Centre+, Maastricht, Netherlands.
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15
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Hudry B, de Goeij E, Mineo A, Gaspar P, Hadjieconomou D, Studd C, Mokochinski JB, Kramer HB, Plaçais PY, Preat T, Miguel-Aliaga I. Sex Differences in Intestinal Carbohydrate Metabolism Promote Food Intake and Sperm Maturation. Cell 2020; 178:901-918.e16. [PMID: 31398343 PMCID: PMC6700282 DOI: 10.1016/j.cell.2019.07.029] [Citation(s) in RCA: 109] [Impact Index Per Article: 21.8] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/29/2018] [Revised: 05/31/2019] [Accepted: 07/15/2019] [Indexed: 02/07/2023]
Abstract
Physiology and metabolism are often sexually dimorphic, but the underlying mechanisms remain incompletely understood. Here, we use the intestine of Drosophila melanogaster to investigate how gut-derived signals contribute to sex differences in whole-body physiology. We find that carbohydrate handling is male-biased in a specific portion of the intestine. In contrast to known sexual dimorphisms in invertebrates, the sex differences in intestinal carbohydrate metabolism are extrinsically controlled by the adjacent male gonad, which activates JAK-STAT signaling in enterocytes within this intestinal portion. Sex reversal experiments establish roles for this male-biased intestinal metabolic state in controlling food intake and sperm production through gut-derived citrate. Our work uncovers a male gonad-gut axis coupling diet and sperm production, revealing that metabolic communication across organs is physiologically important. The instructive role of citrate in inter-organ communication might be significant in more biological contexts than previously recognized.
Intestinal carbohydrate metabolism is male-biased and region-specific Testes masculinize gut sugar handling by promoting enterocyte JAK-STAT signaling The male intestine secretes citrate to the adjacent testes Gut-derived citrate promotes food intake and sperm maturation
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Affiliation(s)
- Bruno Hudry
- MRC London Institute of Medical Sciences, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK; Université Côte d'Azur, CNRS, INSERM, iBV, France.
| | - Eva de Goeij
- MRC London Institute of Medical Sciences, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK
| | - Alessandro Mineo
- MRC London Institute of Medical Sciences, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK
| | - Pedro Gaspar
- MRC London Institute of Medical Sciences, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK
| | - Dafni Hadjieconomou
- MRC London Institute of Medical Sciences, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK
| | - Chris Studd
- MRC London Institute of Medical Sciences, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK
| | - Joao B Mokochinski
- MRC London Institute of Medical Sciences, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK
| | - Holger B Kramer
- MRC London Institute of Medical Sciences, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK
| | - Pierre-Yves Plaçais
- Genes and Dynamics of Memory Systems, Brain Plasticity Unit, CNRS, ESPCI Paris, PSL Research University, 10 rue Vauquelin, 75005 Paris, France
| | - Thomas Preat
- Genes and Dynamics of Memory Systems, Brain Plasticity Unit, CNRS, ESPCI Paris, PSL Research University, 10 rue Vauquelin, 75005 Paris, France
| | - Irene Miguel-Aliaga
- MRC London Institute of Medical Sciences, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0NN, UK.
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16
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Nikanorova AA, Barashkov NA, Nakhodkin SS, Pshennikova VG, Solovyev AV, Romanov GP, Kuzmina SS, Sazonov NN, Burtseva TE, Odland JØ, Fedorova SA. The Role of Leptin Levels in Adaptation to Cold Climates. INTERNATIONAL JOURNAL OF ENVIRONMENTAL RESEARCH AND PUBLIC HEALTH 2020; 17:ijerph17061854. [PMID: 32178438 PMCID: PMC7143756 DOI: 10.3390/ijerph17061854] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Subscribe] [Scholar Register] [Received: 02/12/2020] [Revised: 03/06/2020] [Accepted: 03/10/2020] [Indexed: 12/21/2022]
Abstract
Currently, adipose tissue is considered an endocrine organ that produces hormone-active substances, including leptin, which can play a key role in thermoregulation processes. Therefore, we performed a meta-analysis to investigate the influence of the climatic environment on leptin levels. A systematic literature search in the databases was carried out on 10 January 2020. Finally, 22 eligible articles were included in the current meta-analysis and a total of 13,320 participants were covered in the final analysis. It was shown that males of the “North” subgroup demonstrated significantly higher levels of leptin (10.02 ng/mL; CI: 7.92–12.13) than males of the “South” subgroup (4.9 ng/mL; CI: 3.71–6.25) (p = 0.0001). On the contrary, in the female group, a similar pattern was not detected (p = 0.91). Apparently, in order to maintain body temperature, higher leptin levels are required. The results of the study indicate that such effects are most pronounced in males and to a smaller extent in females, apparently due to a relatively high initial concentration of leptin in females. The correlation between leptin levels and climatic environment data support the hypothesis of leptin-mediated thermoregulation as an adaptive mechanism to cold climates.
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Affiliation(s)
- Alena A. Nikanorova
- Laboratory of Molecular Genetics, Yakut Science Centre of Complex Medical Problems, 677010 Yakutsk, Sakha Republic (Yakutia), Russia; (A.A.N.); (S.S.N.); (V.G.P.); (A.V.S.); (G.P.R.); (S.A.F.)
- Laboratory of Molecular Biology, M.K. Ammosov North-Eastern Federal University, Yakutsk, 677000 Sakha Republic (Yakutia), Russia; (S.S.K.); (N.N.S.)
| | - Nikolay A. Barashkov
- Laboratory of Molecular Genetics, Yakut Science Centre of Complex Medical Problems, 677010 Yakutsk, Sakha Republic (Yakutia), Russia; (A.A.N.); (S.S.N.); (V.G.P.); (A.V.S.); (G.P.R.); (S.A.F.)
- Laboratory of Molecular Biology, M.K. Ammosov North-Eastern Federal University, Yakutsk, 677000 Sakha Republic (Yakutia), Russia; (S.S.K.); (N.N.S.)
- Correspondence:
| | - Sergey S. Nakhodkin
- Laboratory of Molecular Genetics, Yakut Science Centre of Complex Medical Problems, 677010 Yakutsk, Sakha Republic (Yakutia), Russia; (A.A.N.); (S.S.N.); (V.G.P.); (A.V.S.); (G.P.R.); (S.A.F.)
- Laboratory of Molecular Biology, M.K. Ammosov North-Eastern Federal University, Yakutsk, 677000 Sakha Republic (Yakutia), Russia; (S.S.K.); (N.N.S.)
| | - Vera G. Pshennikova
- Laboratory of Molecular Genetics, Yakut Science Centre of Complex Medical Problems, 677010 Yakutsk, Sakha Republic (Yakutia), Russia; (A.A.N.); (S.S.N.); (V.G.P.); (A.V.S.); (G.P.R.); (S.A.F.)
- Laboratory of Molecular Biology, M.K. Ammosov North-Eastern Federal University, Yakutsk, 677000 Sakha Republic (Yakutia), Russia; (S.S.K.); (N.N.S.)
| | - Aisen V. Solovyev
- Laboratory of Molecular Genetics, Yakut Science Centre of Complex Medical Problems, 677010 Yakutsk, Sakha Republic (Yakutia), Russia; (A.A.N.); (S.S.N.); (V.G.P.); (A.V.S.); (G.P.R.); (S.A.F.)
- Laboratory of Molecular Biology, M.K. Ammosov North-Eastern Federal University, Yakutsk, 677000 Sakha Republic (Yakutia), Russia; (S.S.K.); (N.N.S.)
- Laboratory of the Human in the Arctic, The Institute for Humanities Research and Indigenous Studies of the North, Federal Research Center “Yakut Science Center of Siberian Branch of Russian Academy of Science”, Yakutsk, 677027 Sakha Republic (Yakutia), Russia
| | - Georgii P. Romanov
- Laboratory of Molecular Genetics, Yakut Science Centre of Complex Medical Problems, 677010 Yakutsk, Sakha Republic (Yakutia), Russia; (A.A.N.); (S.S.N.); (V.G.P.); (A.V.S.); (G.P.R.); (S.A.F.)
- Laboratory of Molecular Biology, M.K. Ammosov North-Eastern Federal University, Yakutsk, 677000 Sakha Republic (Yakutia), Russia; (S.S.K.); (N.N.S.)
| | - Sargylana S. Kuzmina
- Laboratory of Molecular Biology, M.K. Ammosov North-Eastern Federal University, Yakutsk, 677000 Sakha Republic (Yakutia), Russia; (S.S.K.); (N.N.S.)
| | - Nikolay N. Sazonov
- Laboratory of Molecular Biology, M.K. Ammosov North-Eastern Federal University, Yakutsk, 677000 Sakha Republic (Yakutia), Russia; (S.S.K.); (N.N.S.)
| | - Tatyana E. Burtseva
- Department of Pediatrics and Child Surgery, M.K. Ammosov North-Eastern Federal University, Yakutsk, 677000 Sakha Republic (Yakutia), Russia;
- Laboratory of Monitoring Children Health and Medico-environmental Research, Yakut Science Centre of Complex Medical Problems, Yakutsk, 677010 Sakha Republic (Yakutia), Russia
| | - Jon Øyvind Odland
- Department of Public Health and Nursing, Faculty of Medicine and Health Sciences, NTNU Norwegian University of Science and Technology, 7003 Trondheim, Norway;
| | - Sardana A. Fedorova
- Laboratory of Molecular Genetics, Yakut Science Centre of Complex Medical Problems, 677010 Yakutsk, Sakha Republic (Yakutia), Russia; (A.A.N.); (S.S.N.); (V.G.P.); (A.V.S.); (G.P.R.); (S.A.F.)
- Laboratory of Molecular Biology, M.K. Ammosov North-Eastern Federal University, Yakutsk, 677000 Sakha Republic (Yakutia), Russia; (S.S.K.); (N.N.S.)
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Gewehr MCF, Silverio R, Rosa-Neto JC, Lira FS, Reckziegel P, Ferro ES. Peptides from Natural or Rationally Designed Sources Can Be Used in Overweight, Obesity, and Type 2 Diabetes Therapies. Molecules 2020; 25:E1093. [PMID: 32121443 PMCID: PMC7179135 DOI: 10.3390/molecules25051093] [Citation(s) in RCA: 5] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/15/2020] [Revised: 02/20/2020] [Accepted: 02/25/2020] [Indexed: 12/18/2022] Open
Abstract
Overweight and obesity are among the most prominent health problems in the modern world, mostly because they are either associated with or increase the risk of other diseases such as type 2 diabetes, hypertension, and/or cancer. Most professional organizations define overweight and obesity according to individual body-mass index (BMI, weight in kilograms divided by height squared in meters). Overweight is defined as individuals with BMI from 25 to 29, and obesity as individuals with BMI ≥30. Obesity is the result of genetic, behavioral, environmental, physiological, social, and cultural factors that result in energy imbalance and promote excessive fat deposition. Despite all the knowledge concerning the pathophysiology of obesity, which is considered a disease, none of the existing treatments alone or in combination can normalize blood glucose concentration and prevent debilitating complications from obesity. This review discusses some new perspectives for overweight and obesity treatments, including the use of the new orally active cannabinoid peptide Pep19, the advantage of which is the absence of undesired central nervous system effects usually experienced with other cannabinoids.
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Affiliation(s)
- Mayara C. F. Gewehr
- Department of Pharmacology, Biomedical Sciences Institute, University of São Paulo (USP), São Paulo 05508-000, Brazil;
| | - Renata Silverio
- Department of Pharmacology, Center of Biological Sciences, Federal University of Santa Catarina (UFSC), Florianópolis 88040-900, Brazil;
| | - José Cesar Rosa-Neto
- Department of Cell and Developmental Biology, Biomedical Sciences Institute, University of São Paulo (USP), São Paulo 05508-000, Brazil;
| | - Fabio S. Lira
- Department of Physical Education, São Paulo State University (UNESP), Presidente Prudente 19060-900, Brazil;
| | - Patrícia Reckziegel
- Department of Pharmacology, National Institute of Pharmacology and Molecular Biology (INFAR), Federal University of São Paulo (UNIFESP), São Paulo 05508-000, Brazil;
| | - Emer S. Ferro
- Department of Pharmacology, Biomedical Sciences Institute, University of São Paulo (USP), São Paulo 05508-000, Brazil;
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18
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Kolić I, Stojković L, Dinčić E, Jovanović I, Stanković A, Živković M. Expression of LEP, LEPR and PGC1A genes is altered in peripheral blood mononuclear cells of patients with relapsing-remitting multiple sclerosis. J Neuroimmunol 2020; 338:577090. [DOI: 10.1016/j.jneuroim.2019.577090] [Citation(s) in RCA: 4] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 07/10/2019] [Revised: 10/01/2019] [Accepted: 10/21/2019] [Indexed: 02/06/2023]
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19
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Thota PN, Zackria S, Sanaka MR, Patil D, Goldblum J, Lopez R, Chak A. Racial Disparity in the Sex Distribution, the Prevalence, and the Incidence of Dysplasia in Barrett's Esophagus. J Clin Gastroenterol 2019; 51:402-406. [PMID: 27306940 PMCID: PMC5159321 DOI: 10.1097/mcg.0000000000000559] [Citation(s) in RCA: 3] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Indexed: 12/13/2022]
Abstract
GOALS Our aim was to study the prevalence of dysplasia and progression to high-grade dysplasia (HGD) and esophageal adenocarcinoma (EAC) in African Americans (AA) with Barrett's esophagus (BE) and compare it with that of non-Hispanic white (NHW) controls. BACKGROUND BE, a precursor of EAC, is a disease of predominantly white men and is uncommon in AA. The prevalence of dysplasia and progression to HGD and EAC in AA patients with BE is not clearly known. STUDY All AA or NHW patients with confirmed BE, that is specialized intestinal metaplasia, seen between 2002 and 2013 at our institution were included. Variables such as age, gender, medication use, the body mass index, the date of endoscopy, the hiatal hernia size, the BE length, and histologic findings were noted. Progression to HGD/EAC was evaluated. RESULTS Fifty-two AA and 2394 NHW patients with BE were identified. There was a higher percentage of women in the AA cohort (46.2%) than in the NHW cohort (24.9%, P<0.001). Nondysplastic BE was more prevalent in AA than in NHW (80.8% vs. 68.4%, P=0.058). In the surveillance cohort of 20 AA and 991 NHW, no racial differences in progression to HGD/EAC were observed during a median follow-up of 43 months. CONCLUSIONS This study includes the largest number of AA with histologically confirmed BE reported so far. About 46.2% of the AA cohort with BE in our study consisted of women. There was a trend toward a higher prevalence of nondysplastic BE in AA compared with NHW.
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Affiliation(s)
- Prashanthi N. Thota
- Department of Gastroenterology and Hepatology, Cleveland Clinic, Cleveland, USA
| | - Shamiq Zackria
- Department of Gastroenterology and Hepatology, Cleveland Clinic, Cleveland, USA
| | | | - Deepa Patil
- Department of Pathology, Cleveland Clinic, Cleveland, USA
| | - John Goldblum
- Department of Pathology, Cleveland Clinic, Cleveland, USA
| | - Rocio Lopez
- Department of Biostatistics, Cleveland Clinic, Cleveland, USA
| | - Amitabh Chak
- Department of Gastroenterology, University Hospitals, Cleveland, USA
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20
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Leptin, hsCRP, TNF-α and IL-6 levels from normal aging to dementia: Relationship with cognitive and functional status. J Clin Neurosci 2018; 56:150-155. [DOI: 10.1016/j.jocn.2018.08.027] [Citation(s) in RCA: 24] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/11/2018] [Accepted: 08/13/2018] [Indexed: 01/18/2023]
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21
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Dearden L, Bouret SG, Ozanne SE. Sex and gender differences in developmental programming of metabolism. Mol Metab 2018; 15:8-19. [PMID: 29773464 PMCID: PMC6066743 DOI: 10.1016/j.molmet.2018.04.007] [Citation(s) in RCA: 249] [Impact Index Per Article: 35.6] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 03/26/2018] [Revised: 04/20/2018] [Accepted: 04/23/2018] [Indexed: 12/26/2022] Open
Abstract
BACKGROUND The early life environment experienced by an individual in utero and during the neonatal period is a major factor in shaping later life disease risk-including susceptibility to develop obesity, diabetes, and cardiovascular disease. The incidence of metabolic disease is different between males and females. How the early life environment may underlie these sex differences is an area of active investigation. SCOPE OF REVIEW The purpose of this review is to summarize our current understanding of how the early life environment influences metabolic disease risk in a sex specific manner. We also discuss the possible mechanisms responsible for mediating these sexually dimorphic effects and highlight the results of recent intervention studies in animal models. MAJOR CONCLUSIONS Exposure to states of both under- and over-nutrition during early life predisposes both sexes to develop metabolic disease. Females seem particularly susceptible to develop increased adiposity and disrupted glucose homeostasis as a result of exposure to in utero undernutrition or high sugar environments, respectively. The male placenta is particularly vulnerable to damage by adverse nutritional states and this may underlie some of the metabolic phenotypes observed in adulthood. More studies investigating both sexes are needed to understand how changes to the early life environment impact differently on the long-term health of male and female individuals.
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Affiliation(s)
- Laura Dearden
- University of Cambridge Metabolic Research Laboratories and MRC Metabolic Diseases Unit, Wellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Treatment Centre, Addenbrooke's Hospital, Level 4, Box 289, Cambridge, CB2 0QQ, United Kingdom
| | - Sebastien G Bouret
- The Saban Research Institute, Developmental Neuroscience Program & Diabetes and Obesity Program, Center for Endocrinology, Diabetes and Metabolism, Children's Hospital Los Angeles, University of Southern California, Los Angeles, CA, 90027, USA; Inserm, Jean-Pierre Aubert Research Center, U1172, University Lille 2, Lille, 59045, France
| | - Susan E Ozanne
- University of Cambridge Metabolic Research Laboratories and MRC Metabolic Diseases Unit, Wellcome Trust-MRC Institute of Metabolic Science, Addenbrooke's Treatment Centre, Addenbrooke's Hospital, Level 4, Box 289, Cambridge, CB2 0QQ, United Kingdom.
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Hunma S, Ramuth H, Miles-Chan JL, Schutz Y, Montani JP, Joonas N, Dulloo AG. Do gender and ethnic differences in fasting leptin in Indians and Creoles of Mauritius persist beyond differences in adiposity? Int J Obes (Lond) 2017; 42:280-283. [PMID: 28852206 DOI: 10.1038/ijo.2017.213] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.6] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/23/2017] [Revised: 07/26/2017] [Accepted: 07/30/2017] [Indexed: 11/10/2022]
Abstract
Recent body composition studies on the island of Mauritius in young adults belonging to the two main ethnicities-Indians (South Asian descent) and Creoles (African/Malagasy descent)-have shown gender-specific ethnic differences in their body mass index (BMI)-Fat% relationships. We investigated here whether potential gender and ethnic differences in blood leptin would persist beyond that explained by differences in body composition. In healthy young adult Mauritian Indians and Creoles (79 men and 80 women; BMI range: 15-41 kg m-2), we investigated the relationships between fasted serum leptin with BMI, waist circumference (WC), total fat% assessed by deuterium oxide dilution technique and central adiposity (trunk fat%) assessed by abdominal bioimpedance analysis. The results indicate that the greater elevations in leptin-BMI and leptin-WC regression lines in women compared with men, as well as in Indian men compared with Creole men, are abolished when BMI and WC are replaced by total body fat% and trunk fat%, respectively. In women, no significant between-ethnic difference is observed in total body fat%, trunk fat% and serum leptin. Thus, in young adult Mauritians, a population at high risk for later cardiometabolic diseases, the differences in body fat% entirely accounted for the observed gender and ethnic differences in serum leptin.
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Affiliation(s)
- S Hunma
- Obesity Unit, Ministry of Health and Quality of Life, Victoria Hospital, Mauritius.,Division of Medicine/Physiology, Department of Medicine, University of Fribourg, Fribourg, Switzerland
| | - H Ramuth
- Obesity Unit, Ministry of Health and Quality of Life, Victoria Hospital, Mauritius.,Division of Medicine/Physiology, Department of Medicine, University of Fribourg, Fribourg, Switzerland
| | - J L Miles-Chan
- Division of Medicine/Physiology, Department of Medicine, University of Fribourg, Fribourg, Switzerland
| | - Y Schutz
- Division of Medicine/Physiology, Department of Medicine, University of Fribourg, Fribourg, Switzerland
| | - J-P Montani
- Division of Medicine/Physiology, Department of Medicine, University of Fribourg, Fribourg, Switzerland
| | - N Joonas
- Obesity Unit, Ministry of Health and Quality of Life, Victoria Hospital, Mauritius
| | - A G Dulloo
- Division of Medicine/Physiology, Department of Medicine, University of Fribourg, Fribourg, Switzerland
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Gorgey AS, Farkas GJ, Dolbow DR, Khalil RE, Gater DR. Gender Dimorphism in Central Adiposity May Explain Metabolic Dysfunction After Spinal Cord Injury. PM R 2017; 10:338-348. [PMID: 28827208 DOI: 10.1016/j.pmrj.2017.08.436] [Citation(s) in RCA: 17] [Impact Index Per Article: 2.1] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/16/2017] [Revised: 06/20/2017] [Accepted: 08/03/2017] [Indexed: 01/21/2023]
Abstract
BACKGROUND Increase in visceral adipose tissue (VAT) is an independent risk for mortality and other health-related comorbidities. OBJECTIVE To examine the gender differences in VAT and subcutaneous adipose tissue (SAT) cross-sectional areas (CSA) between men and women with chronic spinal cord injury (SCI). The differences in the distribution of central adiposity were used to determine the association of VAT and SAT to metabolic dysfunction after SCI. DESIGN Cross-sectional design. SETTING Hospital-based study. PARTICIPANTS Sixteen individuals (8 men and 8 women) with motor complete SCI were matched based on age, time since injury, and level of injury. METHODS Anthropometrics, dual x-ray absorptiometry (DXA), and magnetic resonance imaging were captured to measure lean mass, fat mass (FM), percentage FM, VAT, and SAT CSAs. Basal metabolic rate was measured, and intravenous glucose tolerance test and lipid panel were performed. MAIN OUTCOME MEASUREMENTS VAT, SAT, and metabolic profile. RESULTS SAT CSA was 1.6 -1.75 times greater in the upper and lower trunks in women compared to men with SCI (P < .05). VAT CSA was 1.8-2.6 times greater in the upper and lower trunks in men compared to women with SCI (P < .05). VAT adjusted to body weight was greater in men compared to women with SCI. High-density lipoprotein cholesterol (HDL-C) was positively related to SAT and negatively related to VAT. Glucose effectiveness was negatively related to lower trunk SAT (r = -0.60, P = .02). HDL-C ratio and triglycerides were positively related to upper VAT, lower VAT, and VAT:SAT ratio. CONCLUSION Magnetic resonance imaging demonstrated that there is a gender dimorphism in central adiposity in persons with chronic SCI. This gender dimorphism in central adipose tissue distribution may explain the higher prevalence of metabolic dysfunction in men with SCI, especially, the decrease in the HDL-C profile. LEVEL OF EVIDENCE IV.
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Affiliation(s)
- Ashraf S Gorgey
- Spinal Cord Injury and Disorders Service, Hunter Holmes McGuire VAMC, 1201 Broad Rock Blvd, Richmond, VA 23249; Virginia Commonwealth University, Department of Physical Medicine & Rehabilitation, Richmond, VA.,Department of Physical Medicine and Rehabilitation, Penn State College of Medicine, Hershey, PA.,School of Kinesiology, University of Southern Mississippi, Hattiesburg, MI.,Spinal Cord Injury and Disorders Service, Hunter Holmes McGuire VAMC, Richmond, VA.,Department of Physical Medicine and Rehabilitation and Department of Public Health Sciences, Penn State College of Medicine, Hershey, PA
| | - Gary J Farkas
- Spinal Cord Injury and Disorders Service, Hunter Holmes McGuire VAMC, 1201 Broad Rock Blvd, Richmond, VA 23249; Virginia Commonwealth University, Department of Physical Medicine & Rehabilitation, Richmond, VA.,Department of Physical Medicine and Rehabilitation, Penn State College of Medicine, Hershey, PA.,School of Kinesiology, University of Southern Mississippi, Hattiesburg, MI.,Spinal Cord Injury and Disorders Service, Hunter Holmes McGuire VAMC, Richmond, VA.,Department of Physical Medicine and Rehabilitation and Department of Public Health Sciences, Penn State College of Medicine, Hershey, PA
| | - David R Dolbow
- Spinal Cord Injury and Disorders Service, Hunter Holmes McGuire VAMC, 1201 Broad Rock Blvd, Richmond, VA 23249; Virginia Commonwealth University, Department of Physical Medicine & Rehabilitation, Richmond, VA.,Department of Physical Medicine and Rehabilitation, Penn State College of Medicine, Hershey, PA.,School of Kinesiology, University of Southern Mississippi, Hattiesburg, MI.,Spinal Cord Injury and Disorders Service, Hunter Holmes McGuire VAMC, Richmond, VA.,Department of Physical Medicine and Rehabilitation and Department of Public Health Sciences, Penn State College of Medicine, Hershey, PA
| | - Refka E Khalil
- Spinal Cord Injury and Disorders Service, Hunter Holmes McGuire VAMC, 1201 Broad Rock Blvd, Richmond, VA 23249; Virginia Commonwealth University, Department of Physical Medicine & Rehabilitation, Richmond, VA.,Department of Physical Medicine and Rehabilitation, Penn State College of Medicine, Hershey, PA.,School of Kinesiology, University of Southern Mississippi, Hattiesburg, MI.,Spinal Cord Injury and Disorders Service, Hunter Holmes McGuire VAMC, Richmond, VA.,Department of Physical Medicine and Rehabilitation and Department of Public Health Sciences, Penn State College of Medicine, Hershey, PA
| | - David R Gater
- Spinal Cord Injury and Disorders Service, Hunter Holmes McGuire VAMC, 1201 Broad Rock Blvd, Richmond, VA 23249; Virginia Commonwealth University, Department of Physical Medicine & Rehabilitation, Richmond, VA.,Department of Physical Medicine and Rehabilitation, Penn State College of Medicine, Hershey, PA.,School of Kinesiology, University of Southern Mississippi, Hattiesburg, MI.,Spinal Cord Injury and Disorders Service, Hunter Holmes McGuire VAMC, Richmond, VA.,Department of Physical Medicine and Rehabilitation and Department of Public Health Sciences, Penn State College of Medicine, Hershey, PA
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24
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Da Silva Martins J, Castro JH, Sainz Rueda NA, dos Reis LM, Jorgetti V, Affonso Moysés RM, Caramori JT. Renal osteodystrophy in the obesity era: Is metabolic syndrome relevant? PLoS One 2017; 12:e0180387. [PMID: 28719612 PMCID: PMC5515407 DOI: 10.1371/journal.pone.0180387] [Citation(s) in RCA: 6] [Impact Index Per Article: 0.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 03/09/2017] [Accepted: 06/14/2017] [Indexed: 11/19/2022] Open
Abstract
BACKGROUND Observational studies have shown a beneficial effect of obesity on bone health; however, most of those studies were not based on bone biopsies. Metabolic syndrome (MetS) could have an effect on bone remodeling. However, there are no data on the effects of MetS in the presence of renal osteodystrophy. OBJECTIVE The aim of this study was to investigate associations between MetS and renal osteodystrophy using the bone histomorphometric turnover-mineralization-volume (TMV) classification. DESIGN, SETTING, PARTICIPANTS & MEASUREMENTS This observational cross-sectional study included 55 hemodialysis patients (28 women/27 men) who were evaluated for MetS and bone histomorphometry. Biochemical parameters included calcium, phosphorus, alkaline phosphatase, intact parathyroid hormone (iPTH), 25-hydroxyvitamin D, free serum leptin, fibroblast growth factor 23 (FGF23), intact osteocalcin, sclerostin (Scl), glucose, insulin, and thyroid hormones. Robust models of multivariate linear regressions were used for the statistical analyses. RESULTS Females had higher iPTH levels (1,143 vs. 358, p = 0.02). Patients with normal bone volume (BV/TV) had a higher prevalence of MetS (73.6% vs. 41.7%, p = 0.02) and higher serum phosphorus, C-terminal FGF23 and insulin levels. The multivariate regression analysis showed that low-density lipoprotein cholesterol (LDL) was positively correlated with bone formation rate (BFR/BS) and negatively associated with mineralization lag time. Bone volume was negatively associated with age but positively associated with MetS. Body mass index (BMI) was not correlated with any of the bone histomorphometric parameters. CONCLUSION Our results suggest that MetS is not a risk factor for low bone volume in hemodialysis patients. Furthermore, BMI alone was not related to bone volume in this population.
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Affiliation(s)
- Janaina Da Silva Martins
- Nephrology, Department of Internal Medicine, Faculdade de Medicina Botucatu Univ. Estadual Paulista-UNESP. Botucatu, Brazil
- Department of Medicine, Universidade Estadual de Maringa, Maringa, Brazil
- * E-mail:
| | - João Henrique Castro
- Nephrology, Department of Internal Medicine, Faculdade de Medicina Botucatu Univ. Estadual Paulista-UNESP. Botucatu, Brazil
| | - Nestor A. Sainz Rueda
- Multidisciplinary Clinical Nutrition Team, Universidade Estadual de Maringa, Maringa, Brazil
| | | | - Vanda Jorgetti
- Nephrology Division, Universidade de São Paulo, São Paulo, Brazil
| | | | - Jacqueline Teixeira Caramori
- Nephrology, Department of Internal Medicine, Faculdade de Medicina Botucatu Univ. Estadual Paulista-UNESP. Botucatu, Brazil
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25
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Different Intestinal Microbial Profile in Over-Weight and Obese Subjects Consuming a Diet with Low Content of Fiber and Antioxidants. Nutrients 2017; 9:nu9060551. [PMID: 28555008 PMCID: PMC5490530 DOI: 10.3390/nu9060551] [Citation(s) in RCA: 33] [Impact Index Per Article: 4.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/18/2017] [Revised: 05/18/2017] [Accepted: 05/23/2017] [Indexed: 02/06/2023] Open
Abstract
Obesity has been related to an increased risk of multiple diseases in which oxidative stress and inflammation play a role. Gut microbiota has emerged as a mediator in this interaction, providing new mechanistic insights at the interface between fat metabolism dysregulation and obesity development. Our aim was to analyze the interrelationship among obesity, diet, oxidative stress, inflammation and the intestinal microbiota in 68 healthy adults (29.4% normal-weight). Diet was assessed through a food frequency questionnaire and converted into nutrients and dietary compounds using food composition tables. The intestinal microbiota was assessed by quantitative PCR, fecal short chain fatty acids by gas chromatography and serum biomarkers by standard protocols. Higher levels of malondialdehyde (MDA), C reactive protein (CRP), serum leptin, glucose, fat percentage and the intestinal Lactobacillus group were found in the obese people. Cluster analysis of body mass index, fat mass, glucose, LDL/HDL ratio, leptin, MDA and CRP classified the subjects into two groups. The levels of the intestinal Bacteroides-Prevotella-Porphyromonas group were lower in the cluster and linked to a higher pro-oxidant and pro-inflammatory status, whose individuals also had lower intake of fruits, dried fruits, and fish. These results could be useful for designing strategies targeted to obesity prevention.
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26
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Malavolti M, Malagoli C, Crespi CM, Brighenti F, Agnoli C, Sieri S, Krogh V, Fiorentini C, Farnetani F, Longo C, Ricci C, Albertini G, Lanzoni A, Veneziano L, Virgili A, Pagliarello C, Feliciani C, Fanti PA, Dika E, Pellacani G, Vinceti M. Glycaemic index, glycaemic load and risk of cutaneous melanoma in a population-based, case-control study. Br J Nutr 2017; 117:432-438. [PMID: 28196548 DOI: 10.1017/s000711451700006x] [Citation(s) in RCA: 10] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
Abstract
Glycaemic index (GI) and glycaemic load (GL) are indicators of dietary carbohydrate quantity and quality and have been associated with increased risk of certain cancers and type 2 diabetes. Insulin resistance has been associated with increased melanoma risk. However, GI and GL have not been investigated for melanoma. We present the first study to examine the possible association of GI and GL with melanoma risk. We carried out a population-based, case-control study involving 380 incident cases of cutaneous melanoma and 719 age- and sex-matched controls in a northern Italian region. Dietary GI and GL were computed for each subject using data from a self-administered, semi-quantitative food frequency questionnaire. We computed the odds ratio (OR) for melanoma according to quintiles of distribution of GL and GL among controls. A direct association between melanoma risk and GL emerged in females (OR 2·38; 95 % CI 1·25, 4·52 for the highest v. the lowest quintile of GL score, P for trend 0·070) but not in males. The association in females persisted in the multivariable analysis after adjusting for several potential confounders. There was no evidence of an association between GI and melanoma risk. GL might be associated with melanoma risk in females.
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Affiliation(s)
- Marcella Malavolti
- 1Department of Biomedical, Metabolic and Neural Sciences,Research Center for Environmental, Genetic, and Nutritional Epidemiology (CREAGEN),University of Modena and Reggio Emilia,41125 Modena,Italy
| | - Carlotta Malagoli
- 1Department of Biomedical, Metabolic and Neural Sciences,Research Center for Environmental, Genetic, and Nutritional Epidemiology (CREAGEN),University of Modena and Reggio Emilia,41125 Modena,Italy
| | - Catherine M Crespi
- 2Department of Biostatistics and Jonsson Comprehensive Cancer Center,University of California Los Angeles Fielding School of Public Health,Los Angeles,CA 90095-1772,USA
| | - Furio Brighenti
- 3Department of Food Science,University of Parma,43121 Parma,Italy
| | - Claudia Agnoli
- 4Epidemiology and Prevention Unit,Fondazione IRCCS Istituto Nazionale dei Tumori,20133 Milan,Italy
| | - Sabina Sieri
- 4Epidemiology and Prevention Unit,Fondazione IRCCS Istituto Nazionale dei Tumori,20133 Milan,Italy
| | - Vittorio Krogh
- 4Epidemiology and Prevention Unit,Fondazione IRCCS Istituto Nazionale dei Tumori,20133 Milan,Italy
| | - Chiara Fiorentini
- 5Dermatologic Unit,University of Modena and Reggio Emilia,41124 Modena,Italy
| | - Francesca Farnetani
- 5Dermatologic Unit,University of Modena and Reggio Emilia,41124 Modena,Italy
| | - Caterina Longo
- 5Dermatologic Unit,University of Modena and Reggio Emilia,41124 Modena,Italy
| | - Cinzia Ricci
- 6Dermatologic Unit,Santa Maria Nuova Hospital-IRCCS,42123 Reggio Emilia,Italy
| | - Giuseppe Albertini
- 6Dermatologic Unit,Santa Maria Nuova Hospital-IRCCS,42123 Reggio Emilia,Italy
| | - Anna Lanzoni
- 7Dermatologic Unit,Bellaria Hospital,40124 Bologna,Italy
| | | | | | | | | | | | - Emi Dika
- 10Dermatologic Unit,University of Bologna,40138 Bologna,Italy
| | - Giovanni Pellacani
- 5Dermatologic Unit,University of Modena and Reggio Emilia,41124 Modena,Italy
| | - Marco Vinceti
- 1Department of Biomedical, Metabolic and Neural Sciences,Research Center for Environmental, Genetic, and Nutritional Epidemiology (CREAGEN),University of Modena and Reggio Emilia,41125 Modena,Italy
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27
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Ball HC, Londraville RL, Prokop JW, George JC, Suydam RS, Vinyard C, Thewissen JGM, Duff RJ. Beyond thermoregulation: metabolic function of cetacean blubber in migrating bowhead and beluga whales. J Comp Physiol B 2017; 187:235-252. [PMID: 27573204 PMCID: PMC5535305 DOI: 10.1007/s00360-016-1029-6] [Citation(s) in RCA: 22] [Impact Index Per Article: 2.8] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/06/2016] [Revised: 06/22/2016] [Accepted: 08/19/2016] [Indexed: 10/21/2022]
Abstract
The processes of lipid deposition and utilization, via the gene leptin (Lep), are poorly understood in taxa with varying degrees of adipose storage. This study examines how these systems may have adapted in marine aquatic environments inhabited by cetaceans. Bowhead (Balaena mysticetus) and beluga whales (Delphinapterus leucas) are ideal study animals-they possess large subcutaneous adipose stores (blubber) and undergo bi-annual migrations concurrent with variations in food availability. To answer long-standing questions regarding how (or if) energy and lipid utilization adapted to aquatic stressors, we quantified variations in gene transcripts critical to lipid metabolism related to season, age, and blubber depth. We predicted leptin tertiary structure conservation and assessed inter-specific variations in Lep transcript numbers between bowheads and other mammals. Our study is the first to identify seasonal and age-related variations in Lep and lipolysis in these cetaceans. While Lep transcripts and protein oscillate with season in adult bowheads reminiscent of hibernating mammals, transcript levels reach up to 10 times higher in bowheads than any other mammal. Data from immature bowheads are consistent with the hypothesis that short baleen inhibits efficient feeding. Lipolysis transcripts also indicate young Fall bowheads and those sampled during Spring months limit energy utilization. These novel data from rarely examined species expand the existing knowledge and offer unique insight into how the regulation of Lep and lipolysis has adapted to permit seasonal deposition and maintain vital blubber stores.
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Affiliation(s)
- H C Ball
- Department of Biology, The University of Akron, 305 Buchtel Ave, Akron, OH, 44325, USA.
- Department of Anatomy and Neurobiology, Northeast Ohio Medical University, 4209 State Route 44, Rootstown, OH, 44272, USA.
| | - R L Londraville
- Department of Biology, The University of Akron, 305 Buchtel Ave, Akron, OH, 44325, USA
| | - J W Prokop
- Department of Biology, The University of Akron, 305 Buchtel Ave, Akron, OH, 44325, USA
- Hudson Alpha Institute for Biotechnology, 601 Genome Way, Huntsville, AL, 35806, USA
| | - John C George
- North Slope Borough Department of Wildlife Management, P.O. Box 69, Barrow, AK, 99723, USA
| | - R S Suydam
- North Slope Borough Department of Wildlife Management, P.O. Box 69, Barrow, AK, 99723, USA
| | - C Vinyard
- Department of Anatomy and Neurobiology, Northeast Ohio Medical University, 4209 State Route 44, Rootstown, OH, 44272, USA
| | - J G M Thewissen
- Department of Anatomy and Neurobiology, Northeast Ohio Medical University, 4209 State Route 44, Rootstown, OH, 44272, USA
| | - R J Duff
- Department of Biology, The University of Akron, 305 Buchtel Ave, Akron, OH, 44325, USA
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Belin de Chantemèle EJ. Sex Differences in Leptin Control of Cardiovascular Function in Health and Metabolic Diseases. ADVANCES IN EXPERIMENTAL MEDICINE AND BIOLOGY 2017; 1043:87-111. [DOI: 10.1007/978-3-319-70178-3_6] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.8] [Reference Citation Analysis] [Track Full Text] [Subscribe] [Scholar Register] [Indexed: 12/12/2022]
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Babic A, Bao Y, Qian ZR, Yuan C, Giovannucci EL, Aschard H, Kraft P, Amundadottir LT, Stolzenberg-Solomon R, Morales-Oyarvide V, Ng K, Stampfer MJ, Ogino S, Buring JE, Sesso HD, Gaziano JM, Rifai N, Pollak MN, Anderson ML, Cochrane BB, Luo J, Manson JE, Fuchs CS, Wolpin BM. Pancreatic Cancer Risk Associated with Prediagnostic Plasma Levels of Leptin and Leptin Receptor Genetic Polymorphisms. Cancer Res 2016; 76:7160-7167. [PMID: 27780823 PMCID: PMC5181854 DOI: 10.1158/0008-5472.can-16-1699] [Citation(s) in RCA: 40] [Impact Index Per Article: 4.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 06/22/2016] [Revised: 09/21/2016] [Accepted: 10/01/2016] [Indexed: 12/27/2022]
Abstract
Leptin is an adipokine involved in regulating energy balance, which has been identified as a potential biologic link in the development of obesity-associated cancers, such as pancreatic cancer. In this prospective, nested case-control study of 470 cases and 1,094 controls from five U.S. cohorts, we used conditional logistic regression to evaluate pancreatic cancer risk by prediagnostic plasma leptin, adjusting for race/ethnicity, diabetes, body mass index, physical activity, plasma C-peptide, adiponectin, and 25-hydroxyvitamin D. Because of known differences in leptin levels by gender, analyses were conducted separately for men and women. We also evaluated associations between 32 tagging SNPs in the leptin receptor (LEPR) gene and pancreatic cancer risk. Leptin levels were higher in female versus male control participants (median, 20.8 vs. 6.7 ng/mL; P < 0.0001). Among men, plasma leptin was positively associated with pancreatic cancer risk and those in the top quintile had a multivariable-adjusted OR of 3.02 [95% confidence interval (CI), 1.27-7.16; Ptrend = 0.02] compared with men in the bottom quintile. Among women, circulating leptin was not associated with pancreatic cancer risk (Ptrend = 0.21). Results were similar across cohorts (Pheterogeneity = 0.88 for two male cohorts and 0.35 for three female cohorts). In genetic analyses, rs10493380 in LEPR was associated with increased pancreatic cancer risk among women, with an OR per minor allele of 1.54 (95% CI, 1.18-2.02; multiple hypothesis-corrected P = 0.03). No SNPs were significantly associated with risk in men. In conclusion, higher prediagnostic levels of plasma leptin were associated with an elevated risk of pancreatic cancer among men, but not among women. Cancer Res; 76(24); 7160-7. ©2016 AACR.
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Affiliation(s)
- Ana Babic
- Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts
| | - Ying Bao
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts
| | - Zhi Rong Qian
- Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts
| | - Chen Yuan
- Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts
| | - Edward L Giovannucci
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts
- Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts
- Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts
| | - Hugues Aschard
- Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts
| | - Peter Kraft
- Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts
- Department of Biostatistics, Harvard T.H. Chan School of Public Health, Boston, Massachusetts
| | - Laufey T Amundadottir
- Laboratory of Translational Genomics, Division of Cancer Epidemiology and Genetics, National Cancer Institute, NIH, Bethesda, Maryland
| | | | | | - Kimmie Ng
- Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts
| | - Meir J Stampfer
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts
- Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts
- Department of Nutrition, Harvard T.H. Chan School of Public Health, Boston, Massachusetts
| | - Shuji Ogino
- Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts
- Division of MPE Molecular Pathological Epidemiology, Department of Pathology, Brigham and Women's Hospital, Boston, Massachusetts
| | - Julie E Buring
- Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts
- Department of Ambulatory Care and Prevention, Harvard Medical School, Boston, Massachusetts
| | - Howard D Sesso
- Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts
- Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts
| | - John Michael Gaziano
- Division of Preventive Medicine, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts
- Massachusetts Veterans Epidemiology Research and Information Center (MAVERIC), VA Boston Healthcare System, Boston, Massachusetts
| | - Nader Rifai
- Department of Laboratory Medicine, Children's Hospital Boston, Boston, Massachusetts
| | - Michael N Pollak
- Cancer Prevention Research Unit, Department of Oncology, Faculty of Medicine, McGill University, Montreal, Quebec, Canada
| | - Matthew L Anderson
- Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, Texas
| | | | - Juhua Luo
- Department of Community Medicine, West Virginia University, Morgantown, West Virginia
| | - JoAnn E Manson
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts
- Department of Epidemiology, Harvard T.H. Chan School of Public Health, Boston, Massachusetts
- Cancer Prevention Research Unit, Department of Oncology, Faculty of Medicine, McGill University, Montreal, Quebec, Canada
| | - Charles S Fuchs
- Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts
- Channing Division of Network Medicine, Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School, Boston, Massachusetts
| | - Brian M Wolpin
- Department of Medical Oncology, Dana-Farber Cancer Institute, Boston, Massachusetts.
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Abstract
The world is experiencing an epidemic of obesity and its concomitant health problems. One implication is that the normally robust negative feedback system that controls energy homeostasis must be responding to different inputs than in the past. In this review we discuss the influence of gender on the efficacy of adiposity hormones as they interact with food intake control systems in the brain. Specifically, the levels of insulin and leptin in the blood are correlated with body fat, insulin being related mainly to visceral fat and leptin to subcutaneous fat. Since females carry more fat subcutaneously and males carry more fat viscerally, leptin correlates better with total body fat in females and insulin correlates better in males. High visceral fat and plasma insulin are also risk factors for the complications of obesity, including type-2 diabetes, cardiovascular problems, and certain cancers, and these are more prevalent in males. Consistent with these systemic differences, the brains of females are more sensitive to the catabolic actions of low doses of leptin whereas the brains of males are more sensitive to the catabolic action of low doses of insulin. The implications of this are discussed.
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Affiliation(s)
- Stephen C Woods
- Department of Psychiatry, University of Cincinnati, Cincinnati, Ohio 45267, USA.
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Laml T, Hartmann BW, Ruecklinger E, Preyer O, Soeregi G, Wagenbichler P. Maternal Serum Leptin Concentrations Do Not Correlate With Cord Blood Leptin Concentrations in Normal Pregnancy. ACTA ACUST UNITED AC 2016. [DOI: 10.1177/107155760100800108] [Citation(s) in RCA: 9] [Impact Index Per Article: 1.0] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/30/2022]
Affiliation(s)
- Thomas Laml
- Department of Obstetrics and Gynecology, Division of Gynecology, Division of Special Gynecology, University of Vienna Medical School, Vienna, Austria; Institute of Statistical Analyses, Vienna, Austria; University of Vienna Medical School, Institute of Medical and Chemical Laboratories, Vienna, Austria; Ignaz-Semmelweis-Frauenklinik der Stadt Wien, Vienna, Austria
| | | | | | | | | | - Peter Wagenbichler
- Department of Obstetrics and Gynecology, Division of Gynecology, Division of Special Gynecology, University of Vienna Medical School, Vienna, Austria; Institute of Statistical Analyses, Vienna, Austria; University of Vienna Medical School, Institute of Medical and Chemical Laboratories, Vienna, Austria; Ignaz-Semmelweis-Frauenklinik der Stadt Wien, Vienna, Austria
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Rubino E, Vacca A, Govone F, Gai A, Boschi S, Zucca M, De Martino P, Gentile S, Pinessi L, Rainero I. Investigating the role of adipokines in chronic migraine. Cephalalgia 2016; 37:1067-1073. [DOI: 10.1177/0333102416665871] [Citation(s) in RCA: 18] [Impact Index Per Article: 2.0] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Indexed: 12/24/2022]
Abstract
Background and aims Adiponectin, leptin, and resistin are adipocyte-derived secretory factors involved in endothelial function, weight, inflammation, and insulin resistance. Recent studies suggested a role for adipokines in episodic migraine as mediators of inflammatory processes. The aim of this study was to investigate plasma concentrations of adiponectin, leptin, and resistin in patients with chronic migraine. Materials and methods Twenty-seven chronic migraineurs (20 females, 7 males; mean age 49.0 ± 9.0 yrs) and 37 healthy controls (23 females, 14 males; mean age 49.8 ± 15.0 yrs) were selected for the study. Fasting plasmatic levels of total adiponectin, leptin, and resistin were measured using ELISA kits during a pain-free period. Fasting glucose, insulin, total and HDL-cholesterol, triglycerides, and ESR were also determined. Results Serum levels of adiponectin and resistin were significantly increased in chronic migraineurs in comparison with controls ( p = 0.001 and p = 0.032, respectively). After correction for BMI, sex and age, leptin levels were significantly increased in chronic migraineurs ( p = 0.007). A positive correlation between leptin concentrations and both indices of insulin resistance and markers of inflammation was found. Discussion Our data suggest that adiponectin and resistin are altered in non-obese chronic migraineurs. Further studies are needed to elucidate the neurobiological mechanisms underlying adipokine dysfunction in migraine.
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Affiliation(s)
- Elisa Rubino
- Neurology I – Headache Center, Rita Levi Montalcini Department of Neuroscience, University of Torino, Italy
| | - Alessandro Vacca
- Neurology I – Headache Center, Rita Levi Montalcini Department of Neuroscience, University of Torino, Italy
| | - Flora Govone
- Neurology I – Headache Center, Rita Levi Montalcini Department of Neuroscience, University of Torino, Italy
| | - Annalisa Gai
- Neurology I – Headache Center, Rita Levi Montalcini Department of Neuroscience, University of Torino, Italy
| | - Silvia Boschi
- Neurology I – Headache Center, Rita Levi Montalcini Department of Neuroscience, University of Torino, Italy
| | - Milena Zucca
- Neurology I – Headache Center, Rita Levi Montalcini Department of Neuroscience, University of Torino, Italy
| | - Paola De Martino
- Neurology I – Headache Center, Rita Levi Montalcini Department of Neuroscience, University of Torino, Italy
| | - Salvatore Gentile
- Department of Neuroscience and Mental Health, A.O.U. Città della Salute e della Scienza, Torino, Italy
| | - Lorenzo Pinessi
- Neurology I – Headache Center, Rita Levi Montalcini Department of Neuroscience, University of Torino, Italy
- Department of Neuroscience and Mental Health, A.O.U. Città della Salute e della Scienza, Torino, Italy
| | - Innocenzo Rainero
- Neurology I – Headache Center, Rita Levi Montalcini Department of Neuroscience, University of Torino, Italy
- Department of Neuroscience and Mental Health, A.O.U. Città della Salute e della Scienza, Torino, Italy
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Abstract
AbstractThe objective of this study was to examine the changes of serum leptin levels in heifers and steers during fattening. Seven steers and seven heifers at 14 months of age were used in the experiment. Live weight and serum leptin levels were determined at 2-month intervals. Initial live weight was greater in steers than heifers and a similar trend of growth was recorded during the experiment. As a result, live weight was higher in the steers than in the heifers during the experiment. Serum leptin concentration in both groups increased during the experiment and reached optimum level at 22 months of age and did not change thereafter. The increase in serum leptin level was more marked in heifers and leptin level was higher (P < 0·05) in heifers than steers between 18 and 26 months of age. The results suggest that serum leptin level increases during fattening in cattle and the trend is possibly affected by gender.
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Abstract
AbstractPlasma leptin concentration shows pulsatility and diurnal rhythm in humans. However, there are few reports concerning the 24-h profile of circulating leptin levels in ruminants. Five crossbred ewes were housed in metabolism cages under a 1-h light-dark cycle. The ewes were offered alfalfa hay daily to meet their energy requirement. Blood samples were collected at 15-min intervals for 24 h. Plasma leptin concentrations were determined using a radioimmunoassay and the profile of plasma leptin levels was analysed by the PULSAR algorithmic program for detecting pulse. Plasma leptin concentration changed in a pulsatile fashion. The mean leptin concentration was 2·93 ng/ml. The mean pulse frequency was 4·8 pulses per day and the mean pulse amplitude was 0·67 ng/ml with an average pulse length of 1:13 h. Plasma leptin level was not affected by feeding or lighting cycle. These results indicate that plasma leptin level in sheep shows pulsatility but diurnal rhythm is not exhibited.
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Nakamura T, Suzuki M, Okada A, Suzuki J, Hasegawa S, Koike H, Hirayama M, Katsuno M, Sobue G. Association of leptin with orthostatic blood pressure changes in Parkinson's disease. Mov Disord 2016; 31:1417-21. [DOI: 10.1002/mds.26678] [Citation(s) in RCA: 15] [Impact Index Per Article: 1.7] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/10/2015] [Revised: 04/12/2016] [Accepted: 04/24/2016] [Indexed: 01/17/2023] Open
Affiliation(s)
- Tomohiko Nakamura
- Department of Neurology; Nagoya University Graduate School of Medicine; Nagoya Japan
- Department of Laboratory Medicine; Nagoya University Hospital; Nagoya Japan
| | - Masashi Suzuki
- Department of Neurology; Nagoya University Graduate School of Medicine; Nagoya Japan
| | - Akinori Okada
- Department of Neurology; Nagoya University Graduate School of Medicine; Nagoya Japan
| | - Junichiro Suzuki
- Department of Neurology; Nagoya University Graduate School of Medicine; Nagoya Japan
| | - Satoru Hasegawa
- Division of Neurogenetics; Nagoya University Graduate School of Medicine; Nagoya Japan
| | - Haruki Koike
- Department of Neurology; Nagoya University Graduate School of Medicine; Nagoya Japan
| | - Masaaki Hirayama
- Department of Neurology; Nagoya University Graduate School of Medicine; Nagoya Japan
- Department of Pathophysiological Laboratory Sciences; Nagoya University Graduate School of Medicine; Nagoya Japan
| | - Masahisa Katsuno
- Department of Neurology; Nagoya University Graduate School of Medicine; Nagoya Japan
| | - Gen Sobue
- Department of Neurology; Nagoya University Graduate School of Medicine; Nagoya Japan
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Chen W, Li Q, Fan Y, Li D, Jiang L, Qiu P, Tang L. Factors Predicting Difficulty of Laparoscopic Low Anterior Resection for Rectal Cancer with Total Mesorectal Excision and Double Stapling Technique. PLoS One 2016; 11:e0151773. [PMID: 26992004 PMCID: PMC4798689 DOI: 10.1371/journal.pone.0151773] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 10/16/2015] [Accepted: 03/03/2016] [Indexed: 01/22/2023] Open
Abstract
BACKGROUND Laparoscopic sphincter-preserving low anterior resection for rectal cancer is a surgery demanding great skill. Immense efforts have been devoted to identifying factors that can predict operative difficulty, but the results are inconsistent. OBJECTIVE Our study was conducted to screen patients' factors to build models for predicting the operative difficulty using well controlled data. METHOD We retrospectively reviewed records of 199 consecutive patients who had rectal cancers 5-8 cm from the anal verge. All underwent laparoscopic sphincter-preserving low anterior resections with total mesorectal excision (TME) and double stapling technique (DST). Data of 155 patients from one surgeon were utilized to build models to predict standardized endpoints (operative time, blood loss) and postoperative morbidity. Data of 44 patients from other surgeons were used to test the predictability of the built models. RESULTS Our results showed prior abdominal surgery, preoperative chemoradiotherapy, tumor distance to anal verge, interspinous distance, and BMI were predictors for the standardized operative times. Gender and tumor maximum diameter were related to the standardized blood loss. Temporary diversion and tumor diameter were predictors for postoperative morbidity. The model constructed for the operative time demonstrated excellent predictability for patients from different surgeons. CONCLUSIONS With a well-controlled patient population, we have built a predictable model to estimate operative difficulty. The standardized operative time will make it possible to significantly increase sample size and build more reliable models to predict operative difficulty for clinical use.
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Affiliation(s)
- Weiping Chen
- Department of Colorectal Surgery, Zhejiang Cancer Hospital, Hangzhou, Zhejiang, 310022, China
- * E-mail:
| | - Qiken Li
- Department of Colorectal Surgery, Zhejiang Cancer Hospital, Hangzhou, Zhejiang, 310022, China
| | - Yongtian Fan
- Department of Colorectal Surgery, Zhejiang Cancer Hospital, Hangzhou, Zhejiang, 310022, China
| | - Dechuan Li
- Department of Colorectal Surgery, Zhejiang Cancer Hospital, Hangzhou, Zhejiang, 310022, China
| | - Lai Jiang
- Department of Colorectal Surgery, Zhejiang Cancer Hospital, Hangzhou, Zhejiang, 310022, China
| | - Pengnian Qiu
- Department of Colorectal Surgery, Zhejiang Cancer Hospital, Hangzhou, Zhejiang, 310022, China
| | - Lilong Tang
- Department of Radiology, Zhejiang Cancer Hospital, Hangzhou, Zhejiang, 310022, China
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Chandar AK, Devanna S, Lu C, Singh S, Greer K, Chak A, Iyer PG. Association of Serum Levels of Adipokines and Insulin With Risk of Barrett's Esophagus: A Systematic Review and Meta-Analysis. Clin Gastroenterol Hepatol 2015; 13:2241-55.e1-4; quiz e179. [PMID: 26188139 PMCID: PMC4827623 DOI: 10.1016/j.cgh.2015.06.041] [Citation(s) in RCA: 34] [Impact Index Per Article: 3.4] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Grants] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 11/19/2014] [Revised: 04/15/2015] [Accepted: 06/17/2015] [Indexed: 02/07/2023]
Abstract
BACKGROUND & AIMS Metabolically active visceral fat may be associated with esophageal inflammation, metaplasia, and neoplasia. We performed a meta-analysis to evaluate the association of serum adipokines and insulin with Barrett's esophagus (BE). METHODS We performed a systematic search of multiple electronic databases, through April 2015, to identify all studies reporting associations between leptin, adiponectin, insulin, insulin resistance, and risk of BE in adults. Comparing the highest study-specific category with the reference category for each hormone, we estimated the summary adjusted odds ratio (aOR) and 95% confidence intervals (CI), using a random effects model. RESULTS We identified 9 observational studies (10 independent cohorts; 1432 patients with BE total, and 3550 control subjects). Meta-analysis revealed that high serum level of leptin was associated with 2-fold higher risk of BE (BE cases vs population control subjects in 5 studies: aOR, 2.23; 95% CI, 1.31-3.78; I(2), 59%). Total serum level of adiponectin was not associated with BE (BE cases vs population control subjects in 5 studies: aOR, 0.79; 95% CI, 0.46-1.34; I(2), 65%), although 1 study observed decreased risk of BE with increased level of low-molecular-weight adiponectin. High serum level of insulin was associated with increased risk of BE (BE cases vs population control subjects in 3 studies: aOR, 1.74; 95% CI, 1.14-2.65; I(2), 0), whereas insulin resistance was not associated with increased risk of BE (BE cases vs gastroesophageal reflux disease control subjects in 2 studies: aOR, 0.98; 95% CI, 0.42-2.30; I(2), 64%). CONCLUSIONS Increased serum levels of leptin and insulin are associated with increased risk of BE, compared with population control subjects. In contrast, increased total serum levels of adiponectin and insulin do not seem to modify BE risk. Well-designed longitudinal studies of incident BE are needed to clarify existing associations of serum adipokines and insulin with BE.
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Affiliation(s)
- Apoorva Krishna Chandar
- Division of Gastroenterology and Liver Diseases, Case Western Reserve University, Cleveland; Digestive Health Institute, University Hospitals Case Medical Center, Cleveland, Ohio
| | - Swapna Devanna
- Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota
| | - Chang Lu
- Division of Gastroenterology and Liver Diseases, Case Western Reserve University, Cleveland
| | - Siddharth Singh
- Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota
| | - Katarina Greer
- Division of Gastroenterology and Liver Diseases, Case Western Reserve University, Cleveland; Digestive Health Institute, University Hospitals Case Medical Center, Cleveland, Ohio
| | - Amitabh Chak
- Division of Gastroenterology and Liver Diseases, Case Western Reserve University, Cleveland; Digestive Health Institute, University Hospitals Case Medical Center, Cleveland, Ohio
| | - Prasad G Iyer
- Division of Gastroenterology and Hepatology, Mayo Clinic, Rochester, Minnesota.
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Abstract
Central obesity is involved in the pathogenesis and progression of Barrett's esophagus to esophageal adenocarcinoma. Involved are likely both mechanical and nonmechanical effects. Mechanical effects of increased abdominal fat cause disruption of the gastroesophageal reflux barrier leading to increased reflux events. Nonmechanical effects may be mediated by inflammation, via classically activated macrophages, pro-inflammatory cytokines, and adipokines such as Leptin, all of which likely potentiate reflux-mediated inflammation. Insulin resistance, associated with central obesity, is also associated with both Barrett's pathogenesis and progression to adenocarcinoma. Molecular pathways activated in obesity, inflammation and insulin resistance overlap with those involved in Barrett's pathogenesis and progression.
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Selvarajan S, Perumalsamy R, Emmadi P, Thiagarajan R, Namasivayam A. Association Between Gingival Crevicular Fluid Leptin Levels and Periodontal Status - A Biochemical Study on Indian Patients. J Clin Diagn Res 2015; 9:ZC48-53. [PMID: 26155562 PMCID: PMC4484154 DOI: 10.7860/jcdr/2015/12335.5941] [Citation(s) in RCA: 5] [Impact Index Per Article: 0.5] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/28/2014] [Accepted: 03/16/2015] [Indexed: 02/04/2023]
Abstract
AIM The present study was carried out to evaluate and compare the gingival crevicular fluid (GCF) concentrations of leptin in periodontally healthy and diseased subjects, to compare GCF leptin levels with respect to Body Mass Index (BMI) among the study groups and essentially to obtain an insight into leptin's possible role in the initiation and progression of periodontal disease. MATERIALS AND METHODS A total of 60 subjects; both males and females, based on their body mass index were selected for the study. They were categorized into three groups of 20 subjects each, based on their periodontal status, as follows: Group I (clinically healthy periodontium); Group II (gingivitis); Group III (chronic periodontitis). GCF samples of 1 μl were collected extra-crevicularly using black color-coded 1-5 μl calibrated volumetric microcapillary pipettes from one site in each person, and samples were analyzed for leptin using a commercially available ELISA kit. RESULTS The concentration of leptin in GCF of patients in Group I (2272.25 pg/mL) was statistically higher (p < 0.001) than in those of Group II (1421.86 pg/mL) and Group III (1160.67 pg/mL). No statistically significant difference was found when comparing the mean values of leptin between BMI groups in each study group. CONCLUSION As periodontal disease progressed, there was a substantial decrease in the gingival crevicular fluid leptin concentration. This suggests a protective role of leptin with regard to periodontal health.
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Affiliation(s)
- Shalini Selvarajan
- Senior Lecturer, Department of Periodontology, Meenakshi Ammal Dental College and Hospital, Alapakkam Main Road, Maduaravoyal, Chennai, India
| | - Rajapriya Perumalsamy
- Senior Lecturer, Department of Periodontology, Meenakshi Ammal Dental College and Hospital, Alapakkam Main Road, Maduaravoyal, Chennai, India
| | - Pamela Emmadi
- Professor, Department of Periodontology, Meenakshi Ammal Dental College and Hospital, Alapakkam Main Road, Maduaravoyal, Chennai, India
| | - Ramakrishnan Thiagarajan
- Professor, Department of Periodontology, Meenakshi Ammal Dental College and Hospital, Alapakkam Main Road, Maduaravoyal, Chennai, India
| | - Ambalavanan Namasivayam
- Professor & HOD, Department of Periodontology, Meenakshi Ammal Dental College and Hospital, Alapakkam Main Road, Maduaravoyal, Chennai, India
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Vicennati V, Garelli S, Rinaldi E, Di Dalmazi G, Pagotto U, Pasquali R. Cross-talk between adipose tissue and the HPA axis in obesity and overt hypercortisolemic states. Horm Mol Biol Clin Investig 2014; 17:63-77. [PMID: 25372731 DOI: 10.1515/hmbci-2013-0068] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/18/2013] [Accepted: 01/17/2014] [Indexed: 01/23/2023]
Abstract
In addition to its roles in providing insulation and mechanical support, adipose tissue (AT) has been recognised as the major site for storage of surplus fuel. Since leptin was discovered, white AT (WAT) has been recognised as an endocrine organ and an important source of biologically active substances with local and/or systemic action called adipokines. The metabolic and endocrine activities of AT are under the control of several hormones: a particular role has been played by glucocorticoids (GC), which able to participate, along with other hormones, both in recruitment of progenitor cells and in differentiation and secretive activities. AT is also able to generate cortisol from cortisone through 11β-hydroxysteroid-dehydrogenase (11β-HSD). There are controversial reports in the literature, showing a hyperactivity of 11β-HSD in obesity. It has been postulated that obesity, particularly the visceral body fat distribution (V-BFD), may be considered a maladaptation to stress exposure, thus leading to hyperactivation of the hypothalamic-pituitary-adrenal (HPA) axis, and higher-than-normal cortisol levels. In this review, we will examine the cross-talk between the HPA axis and AT, their relationship under stressful events, depending on steroid hormones and different adipokine secretions.
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Tan X, Wang X, Chu H, Liu H, Yi X, Xiao Y. SFRP5 correlates with obesity and metabolic syndrome and increases after weight loss in children. Clin Endocrinol (Oxf) 2014; 81:363-9. [PMID: 24330025 DOI: 10.1111/cen.12361] [Citation(s) in RCA: 26] [Impact Index Per Article: 2.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 07/18/2013] [Revised: 08/12/2013] [Accepted: 11/03/2013] [Indexed: 12/11/2022]
Abstract
OBJECTIVE Secreted frizzled-related protein 5 (SFRP5) is a novel anti-inflammatory adipokine, which has been shown as a mediator between obesity and its comorbidities. The aim of this study was to evaluate the associations of SFRP5 with metabolic syndrome (MetS) and the effects of lifestyle interventions on circulating SFRP5 levels in children. DESIGN A cross-sectional study was conducted among 111 obese children and 49 lean controls, and a lifestyle intervention was performed in a subgroup of 31 obese children for 6 months. Anthropometric parameters, clinical data and circulating SFRP5 levels were measured at baseline and after lifestyle intervention. RESULTS Secreted frizzled-related protein 5 was significantly lower in obese children, especially in those with MetS, and negatively correlated with body mass index (BMI), waist circumference and homeostasis model assessment of insulin resistance. Independent of other well-known risk factors, SFRP5 was a significant predictor of MetS in children. In the longitudinal study, lifestyle intervention led to significant weight loss and higher SFRP5 levels. Furthermore, changes in BMI significantly correlated with the rising magnitude of SFRP5. CONCLUSIONS Serum SFRP5 is regulated by weight status and seems to be correlated with metabolic disorders in children.
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Affiliation(s)
- Xinrui Tan
- Department of Pediatrics, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, China
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Мirrakhimov EМ, Kerimkulova AS, Lunegova ОS, Mirrakhimov AE, Nabiev MP, Neronova KV, Bayramukova AA, Alibaeva NT, Satarov N. The association of leptin with dyslipidemia, arterial hypertension and obesity in Kyrgyz (Central Asian nation) population. BMC Res Notes 2014; 7:411. [PMID: 24981337 PMCID: PMC4105887 DOI: 10.1186/1756-0500-7-411] [Citation(s) in RCA: 12] [Impact Index Per Article: 1.1] [Reference Citation Analysis] [Abstract] [Key Words] [MESH Headings] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 01/09/2014] [Accepted: 06/20/2014] [Indexed: 01/15/2023] Open
Abstract
BACKGROUND Leptin, an adipocytokine produced by adipose tissue, along with the traditional cardiometabolic risk factors, contributes to the development of cardiovascular complications. At the same time, ethnic features of adipocytokines have been insufficiently investigated, especially among Asians, who have an increased risk of cardiovascular complications compared with Europeans. Aim of study was to investigate the relationship between leptin levels and age, gender, anthropometric parameters, lipid parameters, arterial hypertension (AH), and obesity in the adult population of ethnic Kyrgyz people living in Central Asia. RESULTS In total, 322 ethnic Kyrgyz (145 men, 177 women) aged ≥ 30 years were studied. Waist and hip circumference, body mass index, blood glucose, lipids, leptin, and homeostatic model assessment were measured. Patients in the upper quartile of leptin levels had high values of BMI, WC, systolic and diastolic blood pressure, glucose, and HOMA index compared with patients with lower leptin levels. The prevalence of metabolic syndrome and AH increased with higher levels of leptin. Leptin positively correlated with BMI, WC, triglycerides, and glucose concentrations in patients of both sexes. According to the multivariate logistic regression analysis, elevated leptin levels increased by 30 times the risk of obesity in men, regardless of the presence of type 2 diabetes, and 17.7 times in women. CONCLUSION Leptin is associated with general and abdominal obesity, dyslipidemia, and insulin resistance in Kyrgyz patients.
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Affiliation(s)
- Erkin М Мirrakhimov
- Kyrgyz State Medical Academy named by I.K. Akhunbaev, Akhunbaev street 92, Bishkek 720020, Kyrgyzstan
- National Centre of Cardiology and Internal medicine named by М. Mirrakhimov, Togolok Moldo 3, Bishkek 720040, Kyrgyzstan
- Kyrgyz-Russian (Slavic University), Kievskaya 44, Bishkek 720040, Kyrgyzstan
| | - Alina S Kerimkulova
- Kyrgyz State Medical Academy named by I.K. Akhunbaev, Akhunbaev street 92, Bishkek 720020, Kyrgyzstan
| | - Оlga S Lunegova
- National Centre of Cardiology and Internal medicine named by М. Mirrakhimov, Togolok Moldo 3, Bishkek 720040, Kyrgyzstan
| | - Aibek E Mirrakhimov
- Kyrgyz State Medical Academy named by I.K. Akhunbaev, Akhunbaev street 92, Bishkek 720020, Kyrgyzstan
| | - Malik P Nabiev
- Kyrgyz State Medical Academy named by I.K. Akhunbaev, Akhunbaev street 92, Bishkek 720020, Kyrgyzstan
| | - Kseniya V Neronova
- Kyrgyz State Medical Academy named by I.K. Akhunbaev, Akhunbaev street 92, Bishkek 720020, Kyrgyzstan
| | - Asiyat A Bayramukova
- Kyrgyz State Medical Academy named by I.K. Akhunbaev, Akhunbaev street 92, Bishkek 720020, Kyrgyzstan
| | - Nazira T Alibaeva
- Kyrgyz-Russian (Slavic University), Kievskaya 44, Bishkek 720040, Kyrgyzstan
| | - Nurdin Satarov
- Kyrgyz State Medical Academy named by I.K. Akhunbaev, Akhunbaev street 92, Bishkek 720020, Kyrgyzstan
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Rocha NP, Scalzo PL, Barbosa IG, de Sousa MS, Morato IB, Vieira ÉLM, Christo PP, Reis HJ, Teixeira AL. Circulating levels of adipokines in Parkinson's disease. J Neurol Sci 2014; 339:64-8. [DOI: 10.1016/j.jns.2014.01.021] [Citation(s) in RCA: 14] [Impact Index Per Article: 1.3] [Reference Citation Analysis] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 11/07/2013] [Revised: 12/18/2013] [Accepted: 01/14/2014] [Indexed: 12/15/2022]
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Lundsgaard AM, Kiens B. Gender differences in skeletal muscle substrate metabolism - molecular mechanisms and insulin sensitivity. Front Endocrinol (Lausanne) 2014; 5:195. [PMID: 25431568 PMCID: PMC4230199 DOI: 10.3389/fendo.2014.00195] [Citation(s) in RCA: 183] [Impact Index Per Article: 16.6] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 09/04/2014] [Accepted: 10/30/2014] [Indexed: 12/23/2022] Open
Abstract
It has become increasingly apparent that substrate metabolism is subject to gender-specific regulation, and the aim of this review is to outline the available evidence of molecular gender differences in glucose and lipid metabolism of skeletal muscle. Female sex has been suggested to have a favorable effect on glucose homeostasis, and the available evidence from hyperinsulinemic-euglycemic clamp studies is summarized to delineate whether there is a gender difference in whole-body insulin sensitivity and in particular insulin-stimulated glucose uptake of skeletal muscle. Whether an eventual higher insulin sensitivity of female skeletal muscle can be related to gender-specific regulation of molecular metabolism will be topic for discussion. Gender differences in muscle fiber type distribution and substrate availability to and in skeletal muscle are highly relevant for substrate metabolism in men and women. In particular, the molecular machinery for glucose and fatty acid oxidative and storage capacities in skeletal muscle and its implications for substrate utilization during metabolic situations of daily living are discussed, emphasizing their relevance for substrate choice in the fed and fasted state, and during periods of physical activity and recovery. Together, handling of carbohydrate and lipids and regulation of their utilization in skeletal muscle have implications for whole-body glucose homeostasis in men and women. 17-β estradiol is the most important female sex hormone, and the identification of estradiol receptors in skeletal muscle has opened for a role in regulation of substrate metabolism. Also, higher levels of circulating adipokines as adiponectin and leptin in women and their implications for muscle metabolism will be considered.
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Affiliation(s)
- Anne-Marie Lundsgaard
- Section of Molecular Physiology, Department of Nutrition, Exercise and Sports, August Krogh Centre, University of Copenhagen, Copenhagen, Denmark
| | - Bente Kiens
- Section of Molecular Physiology, Department of Nutrition, Exercise and Sports, August Krogh Centre, University of Copenhagen, Copenhagen, Denmark
- *Correspondence: Bente Kiens, Section of Molecular Physiology, Department of Nutrition, Exercise and Sports, August Krogh Centre, University of Copenhagen, Universitetsparken 13, Copenhagen 2100, Denmark e-mail:
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Fuente-Martín E, Argente-Arizón P, Ros P, Argente J, Chowen JA. Sex differences in adipose tissue: It is not only a question of quantity and distribution. Adipocyte 2013; 2:128-34. [PMID: 23991358 PMCID: PMC3756100 DOI: 10.4161/adip.24075] [Citation(s) in RCA: 97] [Impact Index Per Article: 8.1] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 01/31/2013] [Revised: 02/21/2013] [Accepted: 02/21/2013] [Indexed: 12/12/2022] Open
Abstract
Obesity and its associated secondary complications are active areas of investigation in search of effective treatments. As a result of this intensified research numerous differences between males and females at all levels of metabolic control have come to the forefront. These differences include not only the amount and distribution of adipose tissue, but also differences in its metabolic capacity and functions between the sexes. Here, we review some of the recent advances in our understanding of these dimorphisms and emphasize the fact that these differences between males and females must be taken into consideration in hopes of obtaining successful treatments for both sexes.
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Davis KE, D Neinast M, Sun K, M Skiles W, D Bills J, A Zehr J, Zeve D, D Hahner L, W Cox D, M Gent L, Xu Y, V Wang Z, A Khan S, Clegg DJ. The sexually dimorphic role of adipose and adipocyte estrogen receptors in modulating adipose tissue expansion, inflammation, and fibrosis. Mol Metab 2013; 2:227-42. [PMID: 24049737 DOI: 10.1016/j.molmet.2013.05.006] [Citation(s) in RCA: 185] [Impact Index Per Article: 15.4] [Reference Citation Analysis] [Abstract] [Key Words] [Track Full Text] [Journal Information] [Submit a Manuscript] [Subscribe] [Scholar Register] [Received: 04/26/2013] [Revised: 05/22/2013] [Accepted: 05/27/2013] [Indexed: 01/03/2023] Open
Abstract
Our data demonstrate that estrogens, estrogen receptor-α (ERα), and estrogen receptor-β (ERβ) regulate adipose tissue distribution, inflammation, fibrosis, and glucose homeostasis, by determining that αERKO mice have increased adipose tissue inflammation and fibrosis prior to obesity onset. Selective deletion of adipose tissue ERα in adult mice using a novel viral vector technology recapitulated the findings in the total body ERα null mice. Generation of a novel mouse model, lacking ERα specifically from adipocytes (AdipoERα), demonstrated increased markers of fibrosis and inflammation, especially in the males. Additionally, we found that the beneficial effects of estrogens on adipose tissue require adipocyte ERα. Lastly, we determined the role of ERβ in regulating inflammation and fibrosis, by breeding the AdipoERα into the βERKO background and found that in the absence of adipocyte ERα, ERβ has a protective role. These data suggest that adipose tissue and adipocyte ERα protects against adiposity, inflammation, and fibrosis in both males and females.
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Affiliation(s)
- Kathryn E Davis
- Touchstone Diabetes Center, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., K5.252, Dallas, TX 75390-8854, USA
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Elias CF, Purohit D. Leptin signaling and circuits in puberty and fertility. Cell Mol Life Sci 2012; 70:841-62. [PMID: 22851226 PMCID: PMC3568469 DOI: 10.1007/s00018-012-1095-1] [Citation(s) in RCA: 113] [Impact Index Per Article: 8.7] [Reference Citation Analysis] [Abstract] [Track Full Text] [Download PDF] [Journal Information] [Subscribe] [Scholar Register] [Received: 05/24/2012] [Revised: 07/05/2012] [Accepted: 07/09/2012] [Indexed: 12/22/2022]
Abstract
Leptin is an adipocyte-derived hormone involved in a myriad of physiological process, including the control of energy balance and several neuroendocrine axes. Leptin-deficient mice and humans are obese, diabetic, and display a series of neuroendocrine and autonomic abnormalities. These individuals are infertile due to a lack of appropriate pubertal development and inadequate synthesis and secretion of gonadotropins and gonadal steroids. Leptin receptors are expressed in many organs and tissues, including those related to the control of reproductive physiology (e.g., the hypothalamus, pituitary gland, and gonads). In the last decade, it has become clear that leptin receptors located in the brain are major players in most leptin actions, including reproduction. Moreover, the recent development of molecular techniques for brain mapping and the use of genetically modified mouse models have generated crucial new findings for understanding leptin physiology and the metabolic influences on reproductive health. In the present review, we will highlight the new advances in the field, discuss the apparent contradictions, and underline the relevance of this complex physiological system to human health. We will focus our review on the hypothalamic circuitry and potential signaling pathways relevant to leptin’s effects in reproductive control, which have been identified with the use of cutting-edge technologies of molecular mapping and conditional knockouts.
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Affiliation(s)
- Carol F Elias
- Division of Hypothalamic Research, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Y6-220B, Dallas, TX, 75390-9077, USA.
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Telenga ED, Tideman SW, Kerstjens HAM, Hacken NHTT, Timens W, Postma DS, van den Berge M. Obesity in asthma: more neutrophilic inflammation as a possible explanation for a reduced treatment response. Allergy 2012; 67:1060-8. [PMID: 22686834 DOI: 10.1111/j.1398-9995.2012.02855.x] [Citation(s) in RCA: 167] [Impact Index Per Article: 12.8] [Reference Citation Analysis] [Abstract] [MESH Headings] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Accepted: 05/05/2012] [Indexed: 11/29/2022]
Abstract
BACKGROUND The incidence of asthma and obesity is increasing worldwide, and reports suggest that obese patients have more severe asthma. We investigated whether obese asthma patients have more severe airway obstruction and airway hyper-responsiveness and a different type of airway inflammation than lean asthmatics. Furthermore, we assessed the effect of obesity on corticosteroid treatment response. METHODS Patient data from four well-documented asthma cohorts were pooled (n = 423). We evaluated FEV(1) , bronchial hyper-responsiveness (PC(20) ) to either methacholine/histamine or adenosine 5'-monophosphate (AMP) (differential) cell counts in induced sputum and blood and corticosteroid treatment response in 118 patients. RESULTS At baseline, FEV(1) , PC(20) methacholine or histamine, and PC(20) AMP values were comparable in 63 obese (BMI ≥ 30 kg/m(2) ) and 213 lean patients (BMI <25 kg/m(2) ). Obese patients had significantly higher blood neutrophils. These higher blood neutrophils were only seen in obese women and not in obese men. After a two-week treatment with corticosteroids, we observed less corticosteroid-induced improvement in FEV(1) %predicted in obese patients than in lean patients (median 1.7% vs 6.3% respectively, P = 0.04). The percentage of sputum eosinophils improved significantly less with higher BMI (P = 0.03), and the number of blood neutrophils increased less in obese than in lean patients (0.32 x10(3) /μl vs 0.57 x10(3) /μl, P = 0.046). CONCLUSIONS We found no differences in asthma severity between obese and nonobese asthmatics. Interestingly, obese patients demonstrated more neutrophils in sputum and blood than nonobese patients. The smaller improvement in FEV(1) and sputum eosinophils suggests a worse corticosteroid treatment response in obese asthmatics.
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Affiliation(s)
- E D Telenga
- Department of Pulmonology, University of Groningen, University Medical Center Groningen, Groningen, the Netherlands
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The balance between leptin and adiponectin in the control of carcinogenesis - focus on mammary tumorigenesis. Biochimie 2012; 94:2164-71. [PMID: 22728769 DOI: 10.1016/j.biochi.2012.06.013] [Citation(s) in RCA: 56] [Impact Index Per Article: 4.3] [Reference Citation Analysis] [Abstract] [Track Full Text] [Journal Information] [Subscribe] [Scholar Register] [Received: 04/11/2012] [Accepted: 06/08/2012] [Indexed: 12/28/2022]
Abstract
A number of studies indicate that a growing list of cancers may be influenced by obesity. In obese individuals these cancers can be more frequent and more aggressive resulting in reduced survival. One of the most prominent and well characterized cancers in this regard is breast cancer. Obesity plays a complex role in breast cancer and is associated with increased inflammation, angiogenesis and alterations in serum levels of potential growth factors such as insulin, adiponectin, leptin and estrogen. Reduced levels of serum adiponectin have been reported in breast cancer patients compared to healthy controls, particularly in postmenopausal women and the level of adiponectin has been shown to be inversely associated with insulin resistance. The role of serum leptin levels in breast cancer appears to be more complex. Some studies have shown leptin to be increased in women with breast cancer but other studies have found leptin to be decreased or unchanged. This may be due to a number of confounding issues. We and others propose that it may be the levels of adiponectin and leptin as well as the balance of adiponectin and leptin that are the critical factors in breast and other obesity related cancer tumorigenesis. This review will focus on the current understanding of the interplay between obesity and the functions of leptin and adiponectin. It will then examine what is known about their potential roles in cancer particularly as pertains to breast cancer and how the ratio of adiponectin to leptin may play a role in tumorigenesis.
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Chen X, McClusky R, Chen J, Beaven SW, Tontonoz P, Arnold AP, Reue K. The number of x chromosomes causes sex differences in adiposity in mice. PLoS Genet 2012; 8:e1002709. [PMID: 22589744 PMCID: PMC3349739 DOI: 10.1371/journal.pgen.1002709] [Citation(s) in RCA: 252] [Impact Index Per Article: 19.4] [Reference Citation Analysis] [Abstract] [MESH Headings] [Grants] [Track Full Text] [Download PDF] [Figures] [Journal Information] [Subscribe] [Scholar Register] [Received: 12/27/2011] [Accepted: 03/28/2012] [Indexed: 12/12/2022] Open
Abstract
Sexual dimorphism in body weight, fat distribution, and metabolic disease has been attributed largely to differential effects of male and female gonadal hormones. Here, we report that the number of X chromosomes within cells also contributes to these sex differences. We employed a unique mouse model, known as the “four core genotypes,” to distinguish between effects of gonadal sex (testes or ovaries) and sex chromosomes (XX or XY). With this model, we produced gonadal male and female mice carrying XX or XY sex chromosome complements. Mice were gonadectomized to remove the acute effects of gonadal hormones and to uncover effects of sex chromosome complement on obesity. Mice with XX sex chromosomes (relative to XY), regardless of their type of gonad, had up to 2-fold increased adiposity and greater food intake during daylight hours, when mice are normally inactive. Mice with two X chromosomes also had accelerated weight gain on a high fat diet and developed fatty liver and elevated lipid and insulin levels. Further genetic studies with mice carrying XO and XXY chromosome complements revealed that the differences between XX and XY mice are attributable to dosage of the X chromosome, rather than effects of the Y chromosome. A subset of genes that escape X chromosome inactivation exhibited higher expression levels in adipose tissue and liver of XX compared to XY mice, and may contribute to the sex differences in obesity. Overall, our study is the first to identify sex chromosome complement, a factor distinguishing all male and female cells, as a cause of sex differences in obesity and metabolism. Differences exist between men and women in the development of obesity and related metabolic diseases such as type 2 diabetes and cardiovascular disease. Previous studies have focused on the sex-biasing role of hormones produced by male and female gonads, but these cannot account fully for the sex differences in metabolism. We discovered that removal of the gonads uncovers an important genetic determinant of sex differences in obesity—the presence of XX or XY sex chromosomes. We used a novel mouse model to tease apart the effects of male and female gonads from the effects of XX or XY chromosomes. Mice with XX sex chromosomes (relative to XY), regardless of their type of gonad, had increased body fat and ate more food during the sleep period. Mice with two X chromosomes also had accelerated weight gain, fatty liver, and hyperinsulinemia on a high fat diet. The higher expression levels of a subset of genes on the X chromosome that escape inactivation may influence adiposity and metabolic disease. The effect of X chromosome genes is present throughout life, but may become particularly significant with increases in longevity and extension of the period spent with reduced gonadal hormone levels.
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Affiliation(s)
- Xuqi Chen
- Department of Integrative Biology and Physiology and Laboratory of Neuroendocrinology or the Brain Research Institute, University of California Los Angeles, Los Angeles, California, United States of America
| | - Rebecca McClusky
- Department of Integrative Biology and Physiology and Laboratory of Neuroendocrinology or the Brain Research Institute, University of California Los Angeles, Los Angeles, California, United States of America
| | - Jenny Chen
- Department of Human Genetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America
| | - Simon W. Beaven
- Department of Medicine, Division of Digestive Diseases, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America
- Howard Hughes Medical Institute, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America
| | - Peter Tontonoz
- Howard Hughes Medical Institute, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America
- Department of Pathology and Laboratory Medicine, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America
- Molecular Biology Institute, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America
| | - Arthur P. Arnold
- Department of Integrative Biology and Physiology and Laboratory of Neuroendocrinology or the Brain Research Institute, University of California Los Angeles, Los Angeles, California, United States of America
| | - Karen Reue
- Department of Human Genetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America
- Department of Medicine, Division of Digestive Diseases, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America
- Molecular Biology Institute, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, United States of America
- * E-mail:
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