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ROLE of INSULIn RESISTANCE In METABOLIC and cardiovascular diseases

W H-H Sheu, W-J Lee, S-Y Lin, I-T Lee, H-C Ou, L-N Tseng

Division of Endocrinology and Metabolism, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan

It is well established that insulin resistance is a common soil of several metabolic and cardiovascular diseases. This theory was further expanded since the publications of definitions of metabolic syndrome.

Our research group, along with other pioneers, have devoted extensively on various spectrum of insulin resistance and relative disorders. We demonstrated the presence of high prevalence of insulin resistance in nondiabetic subjects with coronary heart disease documented by cardiac angiography. We verified several formulas used for estimation of degree of insulin resistance in nondiabetic individuals. Inflammation, evidenced by higher CRP level, alongs with endothelial dysfunction were identified in diabetic subjects with peripheral vascular diseases. Serum ferritin levels might associate with insulin resistance in nondiabetic women. Subjects with colon polyps and low free thyroxine level tended to have higher chance of metabolic syndrome. Treatment with simvastatin, an HMGCoA reductase inhibitor, reduced fasting as well as postprandial triglyceride levels. Simvastatin also reduced hsCRP level in type 2 diabetes with hypercholesterolemia. Rosuvastatin affected ADMA, a NOS inhibitors, in additional to its powerful LDL cholesterol lowering effects.

Elevated circulating homocysteine levels could be corrected by adding folic acid supplement in obese individuals who underwent weight reduction. Sibutamine treatment had little effect on alteration of serum adiponectin in type 2 diabetes. We characterized several mechanisms, targeting at genes expression of TNF, leptin, resistin, that link to insulin resistance in liver cirrhosis models both in human and rats.

Very recently, we demonstrated that resveratrol, a component of red wine, and rosiglitazone, a commonly used insulin sensitizer, inhibited endothelial proliferation and angiogenesis. Rosiglitazone inhibit endothelial proliferation via interfering cell cycle at G1 phase. We also found that in vitro interaction between monocyte, obtained form nondiabetic individuals, and endothelial cells influenced by serum cholesterol levels rather by presence of metabolic syndrome.