INSULIN SENSITIVITY AND ENDOTHELIAL FUNCTION - A PHYSIOLOGICAL RELATIONSHIP WITH PATHOPHYSIOLOGICAL SIGNIFICANCE

Resistance to insulin-mediated glucose uptake has been consistently sh own in lean hypertensive patients. However, the mechanism responsible for this is unknown. Insulin is a vasodilator hormone and insulin-medi ated vasodilation requires the presence of tissue glucose uptake. The vasodilation is mediated predominantly by endothelial nitric oxide (NO ) production, so that an important interaction between NO and insulin at the level of the endothelium may be relevant to insulin resistance. Poor endothelial function as found in essential hypertension, NIDDM, obesity, heart failure and atherosclerosis appear to be associated wit h decreased insulin-mediated vasodilation and decreased insulin sensit ivity. This indicates that (a) endothelial NO production could determi ne whole body insulin sensitivity by modulating blood flow to insulin sensitive tissue, or that (b) insulin sensitivity could determine endo thelial NO production, or that (c) there could be a common antecedent, either genetic or environmental. (C) 1997, Medikal Press.