Alterations in lipid kinetics in men with HIV-dyslipidemia

Hypertriglyceridemia is common in individuals with human immunodeficiency (HIV) infection, but the mechanisms responsible for increased plasma triglyceride (TG) concentrations are not clear. We evaluated fatty acid and VLDL-TG kinetics during basal conditions and during a glucose infusion that resulted in typical postprandial plasma glucose and insulin concentrations in six men with HIV-dyslipidemia [body mass index (BMI): 28 ± 2 kg/m ²] and six healthy men (BMI: 26 ± 2 kg/m²). VLDL-TG secretion and palmitate rate of appearance (R_a) in plasma were measured by using stable-isotope-labeled tracer techniques. Basal palmitate R_a and VLDL-TG secretion rates were greater (P < 0.01 for both) in men with HIV-dyslipidemia (1.04 ± 0.07 μmol palmitate·kg^-1·min^-1 and 5.7 ± 0.6 μmol VLDL-TG·1 plasma^-1·min^-1) than in healthy men (0.67 ± 0.08 μmol palmitate·kg ^-1·min^-1 and 3.0 ± 0.5 μmol VLDL-TG·1 plasma^-1·min^-1). Basal VLDL-TG plasma clearance was lower in men with HIV-dyslipidemia (13 ± 1 ml/min) than in healthy men (19 ± 2 ml/min; P < 0.05). Glucose infusion decreased palmitate R_a (by ∼50%) and the VLDL-TG secretion rate (by ∼30%) in both groups, but the VLDL-TG secretion rate remained higher (P < 0.05) in subjects with HIV-dyslipidemia. These findings demonstrate that increased secretion of VLDL-TG and decreased plasma VLDL-TG clearance, during both fasting and fed conditions, contribute to hypertriglyceridemia in men with HIV-dyslipidemia. Although it is likely that increased free fatty acid release from adipose tissue contributes to the increase in basal VLDL-TG concentration, other factors must be involved, because insulin-induced suppression of lipolysis and systemic fatty acid availability did not normalize the VLDL-TG secretion rate.