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Adiponectin Multimers and ADIPOQ T45G in Coronary Artery Disease in Caribbean Type 2 Diabetic Subjects of African Descent
Authors:Lydia Foucan  Nabila Ezourhi  Suliya Maimaitiming  Segho Hedreville  Jocelyn Inamo  Andre Atallah  Jacqueline Bangou‐Bredent  Roberte Aubert  Roger Chout  Frederic Fumeron  Jean‐Paul Donnet  Michel Marre
Affiliation:1. EA 4097: Research Group Clinical Epidemiology and Medicine, University of Antilles and Guyane, Pointe‐à‐Pitre, French West Indies;2. Department of Medical Information and Public Health, University Hospital of Pointe‐à‐Pitre, Guadeloupe, French West Indies;3. INSERM U695, Xavier Bichat Medical School, Paris Cedex 18, France;4. Cardiology Unit, University Hospital of Pointe‐à‐Pitre, Guadeloupe, French West Indies;5. Cardiology Unit, University Hospital of Fort‐de‐France, Martinique, French West Indies;6. Cardiology Unit, La Basse‐Terre Hospital, Guadeloupe, French West Indies;7. Diabetology Unit, University Hospital of Pointe‐à‐Pire, Guadeloupe, French West Indies
Abstract:Ethnic differences may affect the association of adiponectin (Ad) multimers with coronary artery disease (CAD). We analyzed the associations of total Ad, Ad multimers, and T45G polymorphism of ADIPOQ gene with pre‐existing CAD. We carried out a cross‐sectional study of 216 Afro‐Caribbean type 2 diabetic (T2D) subjects. Levels of total Ad, high molecular weight (HMW), middle molecular weight (MMW), and low molecular weight (LMW) isoforms were measured. Subjects were genotyped. Of the subjects studied, 57 had pre‐existing CAD, 77% of whom have had myocardial infarction. Subjects with CAD had lower Ad levels (total and multimers) and a higher frequency carried the minor allele 45G, GG/TG, (18% vs. 8%, P = 0.03) than subjects without CAD. In logistic regression analysis, the models used evaluate Ad in the context of adjustment for metabolic syndrome characteristics. The adjusted odds ratio (OR) of CAD was increased significantly (by factors of 1.05–3.27) for males, older subjects, low high‐density lipoprotein cholesterol (HDL‐C), high triglycerides (TGs), and carriers of the 45 G allele. For Ad, in model 1 (including only total Ad) the adjusted OR was 2.30; P = 0.03 and, in model 2 (including the three multimers, but not total Ad), the adjusted ORs were 0.73; P = 0.52 (HMW), 2.90; P = 0.01 (MMW), and 2.08; P = 0.09 (LMW). The T45G polymorphism in the ADIPOQ gene and hypoadiponectinemia were associated with CAD in our T2D subjects of predominantly African background. This effect of Ad level was mainly related to the MMW Ad form.
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