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1 Department of Internal Medicine and Center for Human Nutrition, Washington University School of Medicine, St. Louis, Missouri, USA
* To whom correspondence should be addressed. E-mail: sklein{at}im.wustl.edu.
Hypertriglyceridemia is common in individuals with 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 6 men with HIV-dyslipidemia (body mass index [BMI]: 28 ± 2 kg/m2) and 6 healthy men (BMI: 26 ± 2 kg/m2). VLDL-TG secretion and palmitate rate of appearance (Ra) in plasma were measured by using stable-isotopically labeled tracer techniques. Basal palmitate Ra 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.L plasma-1.min-1) than healthy men (0.67 ± 0.08 µmol palmitate.kg-1.min-1 and 3.0 ± 0.5 µmol VLDL-TG.L plasma-1.min-1). Basal VLDL-TG plasma clearance was lower in men with HIV-dyslipidemia (13 ± 1 mL.min-1) than healthy men (19 ± 2 mL.min-1)(p<0.05). Glucose infusion decreased palmitate Ra (by ~50%) and VLDL-TG secretion rate (by ~30%) in both groups, but 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 FFA 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 VLDL-TG secretion rate.
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