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Mechanisms and Strategies for Insulin Resistance in Acquired Immune Deficiency Syndrome

Steven Grinspoon
Clinical Infectious Diseases
Vol. 37, Supplement 2. Interventions for Metabolic and Endocrine Complications of HIV/AIDS and Drug Abuse (Sep. 1, 2003), pp. S85-S90
Published by: Oxford University Press
Stable URL: http://www.jstor.org/stable/4462557
Page Count: 6
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Mechanisms and Strategies for Insulin Resistance in Acquired Immune Deficiency Syndrome
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Abstract

Abnormalities of glucose regulation, including impaired glucose tolerance and insulin resistance, are often seen among human immunodeficiency virus (HIV)-infected patients receiving highly active antiretroviral therapy. Insulin resistance in this population may result from antiviral medication directly impairing glucose uptake in the muscle, effects of HIV per se, or indirect effects, such as fat redistribution. Insulin resistance may increase the risk of coronary heart disease among this population of patients, in part by inhibiting normal thrombolysis. The optimal treatment for insulin resistance and impaired glucose intolerance in HIV-infected patients is not known, but preliminary studies have suggested that metformin, an insulin sensitizing agent, improves insulin sensitivity, blood pressure, and waist circumference. Initial studies of thiazolidinediones also suggest the potential utility of such agents to improve insulin sensitivity, decrease hepatic steatosis, and increase subcutaneous fat. Further studies are needed to determine the optimal treatment strategy for insulin resistance in this population.

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