Abstract

Statins, as 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase inhibitors, have long been known for having significant effects on plasma lipid and lipoprotein profiles, lowering total and LDL cholesterol and raising HDL-C level. Many studies have previously found that statin therapy reduced the risk of occlusive vascular events in people with diabetes mellitus. In fact, type 2 diabetes is often accompanied by abnormal blood lipid and lipoprotein levels, but most studies on the link between hyperlipidemia and pathogenesis of diabetes have focused on free fatty acids (FFAs), which were believed to enhance hyperglycemia- induced beta cell deterioration and insulin secretion impairment, while the impact of cholesterol in the pathogenesis of diabetes has not been reported. Although the relationship between elevated cholesterol and diabetes has not been extensively examined, there is some evidence supporting a potential link between the two. Firstly, lipoprotein level is closely correlated with the concentration of plasma cholesterol, and the former is a good predictor for onset of diabetes. Secondly, a few clinical studies have indicated that use of statins can delay the progression of diabetes. Though the mechanism underlying this phenomenon is still elusive, it was recently found that elevated serum cholesterol can impair insulin secretion and increase the rate of apoptosis in beta cells, which may offer a promising clue to how statins work.

Keywords: Insulin - secretion, Insulin-Secreting Cells - secretion, Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology, Diabetes Mellitus, Type 2 - prevention & control, Cholesterol - blood, Lipoproteins - blood