Abstract
The pathologies of both obesity and type 2 diabetes (T2DM) involve inflammatory processes that, especially in the coronary vasculature, lead to atherosclerotic lesion formation. The purpose of this study was to examine lesion formation and endothelial adhesion molecule expression in the coronary vasculature of control and type 2 diabetic mice. T2DM was induced in C57BL/6J mice by ad libitum high-fat, high-carbohydrate feeding for 15 weeks. Coronary lesion formation and VCAM-1, ICAM-1 and E-selectin adhesion molecule expression was determined by immunostaining of myocardial sections from both groups. Blood lipid profiles (total cholesterol, triglycerides, HDL and LDL) and glucose tolerance were also determined. Diabetogenic diet fed mice developed obesity, hyperglycemia and hyperinsulinemia characteristic of T2DM. T2DM mice were glucose intolerant with elevated blood glucose levels two hours post challenge (492 ± 43 vs 193 ± 23 mg/dl). All measured blood lipids were elevated in T2DM mice; however, no significant coronary lesions were found in either group. Immunostaining for VCAM-1, but not ICAM-1 or E-selectin, was increased in T2DM coronary vessels. Our results suggest that dyslipidemic type 2 diabetes in this mouse model is characterized by the initial steps of vascular inflammation that may lead to monocyte emigration and atherosclerotic lesion formation. Funded by Ohio Univ. and NIH AR048523-04.
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