Carotid atherosclerosis mediated by visceral adiposity and adipocytokines in type 2 diabetic subjects.

Abstract The aim of this study was to verify the possible association of visceral fat accumulation with carotid atherosclerosis in order to identify the practical and feasible determinants for each parameter of atherosclerosis in type 2 diabetic subjects. The subjects were 151 diabetic (DM) and age-matched 83 nondiabetic subjects (C), without atherosclerotic disease. Visceral fat area (VFA) on a CT scan at the umbilicus level was measured. Ambulatory 24-h blood pressure (BP) was recorded. Stiffness index β, intima–media thickness (IMT) and plaque formation of carotid arteries were measured by ultrasonography. Insulin sensitivity was estimated by homeostasis model assessment (HOMA). Serum levels of adiponectin and tumor necrosis factor (TNF)-α were determined. Male gender, HOMA, serum non-HDL-Cholesterol (Chol) and TNF-α/adiponectin ratio were higher, and VFA was larger in DM than in C. The IMT, stiffness index β and plaque formation in DM were more pronounced than in C, even after adjusting for age, sex and 24-h systolic BP (sBP). VFA was positively correlated with TNF-α/adiponectin ratio and serum non-HDL-Chol in DM. Furthermore, multiple regression analysis revealed that, in DM, serum non-HDL-Chol was associated with IMT, VFA probably via an increase in TNF-α/adiponectin ratio was associated with stiffness index β, and 24-h sBP, HOMA and VFA were associated with plaque formation independently of age and sex, respectively, although any association was not observed in C. Thus, we conclude that visceral fat-associated alterations in adipokines may be mediating the development and progression of atherosclerosis in type 2 diabetic subjects, compared with nondiabetic subjects.