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  • Author: Shane A Norris x
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Philippe Jean-Luc Gradidge Centre for Exercise Science and Sports Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa

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Nicole G Jaff Department of Chemical Pathology, National Health Laboratory Service, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa

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Shane A Norris SAMRC/Wits Developmental Pathways for Health Research Unit, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa
Global Health Research Institute, School of Human Development and Health, University of Southampton, Southampton, UK

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Marketa Toman Department of Chemical Pathology, National Health Laboratory Service, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa

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Nigel J Crowther Department of Chemical Pathology, National Health Laboratory Service, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa

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Gluteofemoral fat correlates negatively with a number of cardiometabolic disease risk factors, but the mechanisms involved in these relationships are unknown. The aim of this study was to test the hypothesis that gluteofemoral fat attenuates the risk of cardiometabolic disease by increasing blood adiponectin levels. This was a cross-sectional study in which arm, leg, gluteofemoral, abdominal s.c. and visceral fat levels were measured by dual-energy X-ray absorptiometry in 648 African females. Fasting serum adiponectin, lipid, insulin and plasma glucose levels and blood pressure were measured. Relationships between variables were analysed using multivariable linear regression and structural equation modelling. Adiponectin correlated positively (β = 0.45, P < 0.0001) with gluteofemoral fat in a multivariable regression model that included age, height, and arm, s.c. and visceral fat levels. In further regression models, there was a negative correlation of gluteofemoral fat with fasting glucose (β = −0.28; P < 0.0001) and triglyceride levels (β = −0.29; P < 0.0001) and insulin resistance (HOMA; β = −0.26; P < 0.0001). Structural equation modelling demonstrated that adiponectin mediated 20.7% (P < 0.01) of the association of gluteofemoral fat with insulin resistance and 16.1% (P < 0.01) of the association with triglyceride levels but only 6.67% (P = 0.31) of the association with glucose levels. These results demonstrate that gluteofemoral and leg fat are positively associated with adiponectin levels and that the negative association of lower body fat with insulin resistance and triglyceride levels may partially be mediated by this adipokine. Further studies are required to determine other factors that mediate the effect of lower body fat on cardiometabolic disease risk factors.

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Siphiwe N Dlamini SAMRC/Wits Developmental Pathways for Health Research Unit (DPHRU), School of Clinical Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa
Non-communicable Diseases Research Unit, South African Medical Research Council, Cape Town, South Africa

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Zané Lombard Division of Human Genetics, National Health Laboratory Service, and School of Pathology, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa

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Lisa K Micklesfield SAMRC/Wits Developmental Pathways for Health Research Unit (DPHRU), School of Clinical Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa

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Nigel Crowther Department of Chemical Pathology, National Health Laboratory Service and Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa

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Shane A Norris SAMRC/Wits Developmental Pathways for Health Research Unit (DPHRU), School of Clinical Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa

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Tracy Snyman Department of Chemical Pathology, National Health Laboratory Service and Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa

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Andrew A Crawford Population Health Sciences, Bristol Medical School, University of Bristol, Bristol, UK
BHF Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK

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Brian R Walker BHF Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, UK
Institute of Genetic Medicine to Translational & Clinical Research Institute, Newcastle University, Newcastle upon Tyne, UK

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Julia H Goedecke SAMRC/Wits Developmental Pathways for Health Research Unit (DPHRU), School of Clinical Medicine, Faculty of Health Sciences, University of the Witwatersrand, Johannesburg, South Africa
Non-communicable Diseases Research Unit, South African Medical Research Council, Cape Town, South Africa

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Circulating glucocorticoids are associated with metabolic syndrome and related cardiometabolic risk factors in non-Africans. This study investigated these associations in Africans, whose metabolic phenotype reportedly differs from Europeans. Adiposity, blood pressure, glycaemia, insulin resistance, and lipid profile, were measured in 316 African men and 788 African women living in Soweto, Johannesburg. The 2009 harmonized criteria were used to define metabolic syndrome. Serum glucocorticoids were measured using liquid chromatography-mass spectrometry. Cortisol was associated with greater odds presenting with metabolic syndrome (odds ratio (95% CI) =1.50 (1.04, 2.17) and higher systolic (beta coefficient, β (95% CI) =0.04 (0.01, 0.08)) and diastolic (0.05 (0.02, 0.09)) blood pressure, but higher HDL (0.10 (0.02, 0.19)) and lower LDL (−0.14 (−0.24, −0.03)) cholesterol concentrations, in the combined sample of men and women. In contrast, corticosterone was only associated with higher insulin sensitivity (Matsuda index; 0.22 (0.03, 0.41)), but this was not independent of BMI. Sex-specific associations were observed, such that both cortisol and corticosterone were associated with higher fasting glucose (standardized β (95% CI): 0.24 (0.12, 0.36) for cortisol and 0.12 (0.01, 0.23) for corticosterone) and HbA1c (0.13 (0.01, 0.25) for cortisol and 0.12 (0.01, 0.24) for corticosterone) in men only, but lower HbA1c (0.10 (−0.20, −0.01) for cortisol and −0.09 (−0.18, −0.03) for corticosterone) in women only. Our study reports for the first time that associations between circulating glucocorticoid concentrations and key cardiometabolic risk factors exhibit both glucocorticoid- and sex-specificity in Africans.

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