A L Borel1, J A Nazare2, J Smith3, P Aschner4, P Barter5, L Van Gaal6, C Eng Tan7, H U Wittchen8, Y Matsuzawa9, T Kadowaki10, R Ross11, C Brulle-Wohlhueter12, N Alméras3, S M Haffner13, B Balkau14, J P Després3. 1. 1] Centre de Recherche de l'Institut Universitaire de Pneumologie et de Cardiologie de Québec, Québec, Quebec, Canada [2] HP2 Laboratory INSERM U1042, Grenoble Alpes University, Grenoble, France [3] Endocrinology Department, University Hospital of Grenoble, Grenoble, France. 2. 1] Centre de Recherche de l'Institut Universitaire de Pneumologie et de Cardiologie de Québec, Québec, Quebec, Canada [2] Centre Européen Nutrition Pour la Santé (CENS), CarMeN Laboratory, Pierre-Bénite, France. 3. Centre de Recherche de l'Institut Universitaire de Pneumologie et de Cardiologie de Québec, Québec, Quebec, Canada. 4. Javeriana University School of Medicine, San Ignacio University Hospital, Bogotá, Colombia. 5. Centre for Vascular Research, Faculty of Medicine, University of New South Wales, Sydney, New South Wales, Australia. 6. Department of Endocrinology, Diabetology, Metabolism and Clinical Nutrition, Antwerp University Hospital, Edegem, Belgium. 7. Gleneagles Medical Centre, SingapRe, Singapore. 8. Institute of Clinical Psychology and Psychotherapy and Center of Clinical Epidemiology and Longitudinal Studies (CELOS), Technische Universitaet Dresden, Dresden, Germany. 9. Department of Endocrinology and Metabolism, Sumitomo Hospital, Osaka, Japan. 10. Department of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. 11. Queen's University, School of Kinesiology and Health Studies, Kingston, Ontario, Canada. 12. Sanofi, Paris, France. 13. Baylor College of Medicine, San Antonio, TX, USA. 14. INSERM, CESP Centre for Research in Epidemiology and Population Health, UMRS 1018, Epidemiology of Diabetes, Obesity and Chronic Kidney Disease over the Lifecourse and Determinants of Early Nutrition, Villejuif; University Paris Sud 11, Paris, France.
Abstract
OBJECTIVES: To examine the specific distribution of liver fat content, visceral and subcutaneous adiposity in normal glucose tolerance (NGT/NGT), isolated impaired fasting glucose (iIFG), isolated impaired glucose tolerance (iIGT) and combined conditions (IFG+IGT), as well as with newly diagnosed type 2 diabetes (nT2D). DESIGN: Multicenter, international observational study: cross-sectional analysis. SUBJECTS: Two thousand five hundred and fifteen patients (50.0% women, 54.5% non-Caucasian) without previously known diabetes were recruited from 29 countries. Abdominal fat distribution was measured by computed tomography (CT). Liver fat was estimated using the CT-liver mean attenuation. RESULTS: Compared with NGT/NGT patients, increased visceral adiposity was found in iIFG, iIGT, IFG+IGT and nT2D; estimated liver fat progressively increased across these conditions. A one-s.d. increase in visceral adiposity was associated with an increased risk of having iIFG (men: odds ratio (OR) 1.41 (95% confidence interval (CI) 1.15-1.74), women: OR 1.62 (1.29-2.04)), iIGT (men: OR 1.59 (1.15-2.01), women: OR 1.30 (0.96-1.76)), IFG+IGT (men: OR 1.64 (1.27-2.13), women: OR 1.83 (1.36-2.48)) and nT2D (men: OR 1.80 (1.35-2.42), women: OR 1.73 (1.25-2.41)). A one-s.d. increase in estimated liver fat was associated with iIGT (men: OR 1.46 (1.12-1.90), women: OR 1.81 (1.41-2.35)), IFG+IGT (men: OR 1.42 (1.14-1.77), women: OR 1.74 (1.35-2.26)) and nT2D (men: OR 1.77 (1.40-2.27), women: OR 2.38 (1.81-3.18)). Subcutaneous abdominal adipose tissue showed an inverse relationship with nT2D in women (OR 0.63 (0.45-0.88)). CONCLUSIONS: Liver fat was associated with iIGT but not with iIFG, whereas visceral adiposity was associated with both. Liver fat and visceral adiposity were associated with nT2D, whereas subcutaneous adiposity showed an inverse relationship with nT2D in women.
OBJECTIVES: To examine the specific distribution of liver fat content, visceral and subcutaneous adiposity in normal glucose tolerance (NGT/NGT), isolated impaired fasting glucose (iIFG), isolated impaired glucose tolerance (iIGT) and combined conditions (IFG+IGT), as well as with newly diagnosed type 2 diabetes (nT2D). DESIGN: Multicenter, international observational study: cross-sectional analysis. SUBJECTS: Two thousand five hundred and fifteen patients (50.0% women, 54.5% non-Caucasian) without previously known diabetes were recruited from 29 countries. Abdominal fat distribution was measured by computed tomography (CT). Liver fat was estimated using the CT-liver mean attenuation. RESULTS: Compared with NGT/NGT patients, increased visceral adiposity was found in iIFG, iIGT, IFG+IGT and nT2D; estimated liver fat progressively increased across these conditions. A one-s.d. increase in visceral adiposity was associated with an increased risk of having iIFG (men: odds ratio (OR) 1.41 (95% confidence interval (CI) 1.15-1.74), women: OR 1.62 (1.29-2.04)), iIGT (men: OR 1.59 (1.15-2.01), women: OR 1.30 (0.96-1.76)), IFG+IGT (men: OR 1.64 (1.27-2.13), women: OR 1.83 (1.36-2.48)) and nT2D (men: OR 1.80 (1.35-2.42), women: OR 1.73 (1.25-2.41)). A one-s.d. increase in estimated liver fat was associated with iIGT (men: OR 1.46 (1.12-1.90), women: OR 1.81 (1.41-2.35)), IFG+IGT (men: OR 1.42 (1.14-1.77), women: OR 1.74 (1.35-2.26)) and nT2D (men: OR 1.77 (1.40-2.27), women: OR 2.38 (1.81-3.18)). Subcutaneous abdominal adipose tissue showed an inverse relationship with nT2D in women (OR 0.63 (0.45-0.88)). CONCLUSIONS: Liver fat was associated with iIGT but not with iIFG, whereas visceral adiposity was associated with both. Liver fat and visceral adiposity were associated with nT2D, whereas subcutaneous adiposity showed an inverse relationship with nT2D in women.
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