Adipose tissue can release proinflammatory mediators, namely C-reactive protein (CRP), interleukin 1β (IL-1β), and monocyte chemotactic protein 1 (MCP-1), contributing to vascular injury and insulin resistance (IR). Other mediators namely, adiponectin and nitric oxide (NO) are protective. We enrolled type 2 diabetes mellitus (T2DM) obese male patients without coronary heart disease ([CHD] group II, n = 25) and T2DM obese patients with CHD (group III, n = 25). They were compared with 20 age- and body mass index (BMI)-matched nondiabetic control males (group I). Fasting blood glucose (FBG), glycated hemoglobin (HbA1c%), lipids, insulin, malondialdehyde ([MDA]; lipid peroxidation product), NO, high-sensitivity CRP (hsCRP), IL-1β, MCP-1, adiponectin as well as sE-selectin concentration were significantly different in patients with T2DM and CHD compared with patients without CHD and nondiabetic controls (P = .01). There was a significant negative correlation between adiponectin and E-selectin (P = .0001). Adipose tissue in T2DM obese patients may contribute to the pathogenesis of CHD.
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