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

Alterations in liver, muscle, and adipose tissue insulin sensitivity in men with HIV infection and dyslipidemia. Am J Physiol Endocrinol Metab 290: E47 - E53, 2006. First published August 23, 2005; doi: 10.1152/ajpendo. 00236.2005. - 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 R-a), glucose disposal (glucose R-d), and lipolysis (palmitate R-a) were similar between groups. The relative suppression of glucose R-a (63 +/- 4, 77 +/- 2, and 78 +/- 3%, P = 0.008) and palmitate R-a (49 +/- 4, 63 +/- 3, and 68 +/- 3%, P = 0.005) during low-dose insulin infusion (plasma insulin similar to 30 mu U/ml), and the relative stimulation of glucose R-d (214 +/- 21, 390 +/- 25, and 393 +/- 46%, P = 0.001) during high-dose insulin infusion (plasma insulin similar to 75 mu U/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.