Insulin Resistance

Together with dyslipidemia, hypertension, and obesity, insulin resistance is a key feature of the metabolic syndrome. In addition, it is the first measurable metabolic disturbance among individuals who will subsequently develop type 2 diabetes. Insulin resistance describes a reduced sensitivity in body tissues to the action of insulin, which affects both glucose disposal in muscles and fat and insulin suppression of hepatic glucose output. As a consequence, higher concentrations of insulin are needed to stimulate peripheral glucose disposal and to suppress hepatic glucose production in patients with type 2 diabetes than those without diabetes. On a biologic level, insulin resistance has been associated with increased coagulation, pro-inflammation, and endothelial dysfunction, among other conditions.10 In insulin-resistant subjects, endothelium-dependent vasodilation is reduced, and the severity of the impairment correlates with the degree of insulin resistance. Abnormal endothelium-dependent vaso-dilation in insulin-resistant states may be explained by alterations in intracellular signaling that reduce the production of nitric oxide (NO). Finally, insulin resistance is associated with elevations in free fatty acid levels, which may also contribute to decreased NO synthase activity and reduced production of NO in insulin-resistant states.11 With respect to the clinical implications, insulin resistance has been associated with an increased CV risk. Recently, even among nondiabetic patients, high fasting plasma insulin was found to be an independent risk factor of long-term mortality in individuals with acute myocardial infarction (MI) and of new onset of heart failure in elderly patients without known heart disease.12,13

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