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Insulin secretion in lipodystrophic HIV-infected patients is associated with high levels of nonglucose secretagogues and insulin resistance of -cells

¹Department of Infectious Diseases, ²Department of Endocrinology and Internal Medicine, and ³Clinical Trial Unit, Hvidovre University Hospital, DK 2650 Copenhagen; ⁴Steno Diabetes Center, Gentofte, DK-2820 Copenhagen; and ⁵Copenhagen Muscle Research Centre and ⁶Department of Medical Physiology, The Panum Institute, University of Copenhagen, DK 2200 Copenhagen, Denmark

Submitted 7 January 2004 ; accepted in final form 6 May 2004

We examined whether plasma concentrations of nonglucose insulin secretagogues are associated with prehepatic insulin secretion rates (ISR) in nondiabetic, insulin-resistant, human immunodeficiency virus (HIV)-infected, lipodystrophic patients (LIPO). Additionally, the negative feedback of insulin on ISR was evaluated. ISR were estimated by deconvolution of plasma C-peptide concentrations during fasting (basal) and during the last 30 min of a 120-min euglycemic insulin clamp (40 mU·m^–2·min^–1). Eighteen normoglycemic LIPO were compared with 25 normoglycemic HIV-infected patients without lipodystrophy (controls). Thirty minutes before start of the clamp, a bolus of glucose was injected intravenously to stimulate endogenous insulin secretion. Insulin sensitivity index (Si_Rd) was estimated from glucose tracer analysis. LIPO displayed increased basal ISR (69%), clamp ISR (114%), basal insulin (130%), and clamp insulin (32%), all P 0.001, whereas Si_Rd was decreased (57%, P < 0.001). In LIPO, ISR_basal correlated significantly with basal insulin, alanine, and glucagon (all r > 0.65, P < 0.01), but not with glucose. In control subjects, ISR_basal correlated significantly with insulin, glucagon, and glucose (all r > 0.41, P < 0.05), but not with alanine. In LIPO, ISR_clamp correlated significantly with clamp free fatty acids (FFA), alanine, triglyceride, and glucagon (all r > 0.51, P < 0.05). In control subjects, ISR_clamp correlated with clamp triglyceride (r = 0.45, P < 0.05). Paradoxically, in LIPO, ISR_clamp correlated positively with clamp insulin (r = 0.68, P < 0.01), which suggests an absent negative feedback of insulin on ISR. Our data support evidence that lipodystrophic, nondiabetic, HIV-infected patients exhibit increased ISR, which can be partially explained by an impaired negative feedback of insulin on -cells and an increased stimulation of ISR by FFA, alanine, triglyceride, and glucagon.

human immunodeficiency virus; nonglucose insulin secretagogues

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