Second World Congress on the Insulin Resistance Syndrome

Abstract

This is the third and final installment in a series of articles on the Second World Congress on the Insulin Resistance Syndrome, Universal City, California, 18–20 November 2004. At a symposium on insulin resistance, hypertension, and cardiovascular disease (CVD) cosponsored by the European Group for the Research of Obesity, Hypertension, and Insulin Resistance, Albert P. Rocchini (Ann Arbor, MI) discussed the relationship of hypertension and insulin resistance in obesity. Potential explanations for the frequency with which insulin resistance and hypertension are associated could be the coincidence of two common abnormalities, the causation of one by the other, or, intriguingly, the existence of a common underlying factor. The first explanation appears unlikely, with a preponderance of evidence suggesting that the two conditions are related (1). It also appears unlikely that hypertension causes insulin resistance, as glucose uptake is not affected in experimental renovascular hypertension and because lowering blood pressure in individuals with hypertension does not necessarily improve glucose uptake. There is, however, greater forearm vascular resistance in obese than in nonobese adolescents, with glucose uptake across this tissue inversely related to vascular resistance, suggesting that vascular resistance may play a role in some aspects of insulin action (2). The converse, that insulin resistance may cause hypertension, appears more likely to be a factor. Fasting insulin levels correlate with systolic blood pressure, and the drop in blood pressure following weight loss is related to the improvement in insulin sensitivity. Interestingly, in hypertensive obese individuals, somatostatin decreases both the insulin level and blood pressure, suggesting an effect of hyperinsulinemia. Insulin can lead to sodium retention (3) and angiotensin II–mediated aldosterone production, can change vascular structure and function, can alter cation flux, and can activate the sympathetic nervous system. In both obese and nonobese individuals during water diuresis, however, sodium excretion decreases with a …