Alterations in liver, muscle, and adipose tissue insulin sensitivity in men with HIV infection and dyslipidemia

D. N. Reeds, K. E. Yarasheski, L. Fontana, W. T. Cade, E. Laciny, A. DeMoss, B. W. Patterson, W. G. Powderly, S. Klein

Research output: Contribution to journalArticlepeer-review

49 Scopus citations

Abstract

Dyslipidemia is common in patients with HIV infection. In this study, a two-stage euglycemic hyperinsulinemic clamp, with infusion of stable isotopically labeled tracers, was used to evaluate insulin action in skeletal muscle, liver, and adipose tissue in HIV-infected men with dyslipidemia (HIV-DL; plasma triglyceride >250 mg/dl and HDL <45mg/dl; n = 12), HIV-infected men without dyslipidemia (HIV w/o DL; n = 12), and healthy men (n = 6). Basal rates of glucose production (glucose Ra), glucose disposal (glucose Rd), and lipolysis (palmitate Ra) were similar between groups. The relative suppression of glucose Ra (63 ± 4, 77 ± 2, and 78 ± 3%, P = 0.008) and palmitate Ra (49 ± 4, 63 ± 3, and 68 ± 3%, P = 0.005) during low-dose insulin infusion (plasma insulin ∼30 μU/ml), and the relative stimulation of glucose Rd (214 ± 21, 390 ± 25, and 393 ± 46%, P = 0.001) during high-dose insulin infusion (plasma insulin ∼75 μU/ml) were lower in HIV-DL than in HIV w/o DL and healthy volunteers, respectively. Suppression of basal glucose Ra correlated with plasma adiponectin (r = 0.44, P = 0.02) and inversely with plasma IL-6 (r = -0.49, P < 0.001). Stimulation of glucose Rd correlated directly with adiponectin (r = 0.48, P < 0.01) and inversely with IL-6 (r = -0.49, P = 0.02). We conclude that dyslipidemia in HIV-infected men is indicative of multiorgan insulin resistance, and circulating adipokines may be important in the pathogenesis of impaired insulin action.

Original languageEnglish
Pages (from-to)E47-E53
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume290
Issue number1
DOIs
StatePublished - Jan 2006

Keywords

  • Adipokine
  • Hepatic steatosis
  • Insulin resistance

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