Insulin Resistance in HIV Protease Inhibitor–Associated Diabetes

摘要: BACKGROUND: Fasting hyperglycemia has been associated with HIV protease inhibitor (PI) therapy. OBJECTIVE: To determine whether absolute insulin deficiency or resistance relative and an elevated body mass index (BMI) contribute to PI-associated diabetes. DESIGN: Cross-sectional evaluation. PATIENTS: 8 healthy seronegative men, 10 nondiabetic HIV-positive patients naive PI, 15 receiving PI (BMI = 26 kg/m2), 6 31 diabetes 34 kg/m2). All on received indinavir. MEASUREMENTS: concentrations of glucoregulatory hormones. Direct effects indinavir (20 microM) rat pancreatic beta-cell function in vitro. RESULTS: In hyperglycemic subjects, circulating insulin, C-peptide, proinsulin, glucagon, the proinsulin/insulin ratio were increased when compared those other 4 groups (p <.05). Morning fasting serum cortisol not different among 5 groups. Glutamic acid decarboxylase (GAD) antibody titers uncommon all High BMI was always vitro, did inhibit proinsulin conversion impair glucose-induced secretion C-peptide from beta-cells. CONCLUSIONS: The pathogenesis involves peripheral hyperglucagonemia a high BMI. Pancreatic impaired by mirrors that non-insulin-dependent mellitus action periphery.