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 [+ or -] 2 kg/[m.sup.2]] and six healthy men (BMI: 26 [+ or -] 2 kg/[m.sup.2]). VLDL-TG secretion and palmitate rate of appearance ([R.sub.a]) in plasma were measured by using stable-isotope-labeled tracer techniques. Basal palmitate [R.sub.a] and VLDL-TG secretion rates were greater (P < 0.01 for both) in men with HIV-dyslipidemia (1.04 [+ or -] 0.07 [micro]mol palmitate*[kg.sup.-1].[min.sup.-1] and 5.7 [+ or -] 0.6 [micro]mol VLDL-TG*l [plasma.sup.-1]*[min.sup.-1]) than in healthy men (0.67 [+ or -] 0.08 [micro]mol palmitate*[kg.sup.-1]*[min.sup.-1] and 3.0 [+ or -] 0.5 [micro]mol VLDL-TG*l [plasma.sup.-1]*[min.sup.-1]). Basal VLDL-TG plasma clearance was lower in men with HIV-dyslipidemia (13 [+ or -]1 ml/min) than in healthy men (19 [+ or -] 2 ml/min; P < 0.05). Glucose infusion decreased palmitate [R.sup.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. stable isotopes; lipolysis; hypertriglyceridemia; metabolism; human immunodeficiency virus