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BACKGROUND: Features of the dyslipidemic pattern reported with the use of antiretroviral therapy predict enhanced postprandial lipemia, which is an emerging cardiovascular disease risk factor. OBJECTIVE: We evaluated the postprandial response to a physiologic, meal-based challenge in HIV-positive subjects without hyperlipidemia. DESIGN: We measured hourly lipid, lipoprotein, glucose, and insulin concentrations during a 13-h period in 25 nonwhite patients (13 women, 12 men): 13 receiving a protease inhibitor (PI)-based regimen (6 nelfinavir and 7 indinavir) and 12 receiving a nonnucleoside reverse transcriptase inhibitor (NNRTI)-based regimen (6 efavirenz and 6 nevirapine). RESULTS: Mean fasting HDL-cholesterol concentrations were lower in HIV patients than in healthy subjects without HIV infection matched for age, sex, and ethnicity (z score: -0.81 +/- 0.9; P = 0.0001). Fasting triacylglycerol concentrations were not significantly different between HIV-infected patients and healthy subjects but were higher in PI-treated than in NNRTI-treated patients [median (interquartile range): 144 (110-191) and 89 (62-135) mg/dL; P = 0.007]. Average daylong triacylglycerol concentrations, but not incremental concentrations, were higher in the PI group than in the NNRTI group [205% (185-248%) and 125% (78-191%); P < 0.05]. For all HIV-positive patients, the fractional triacylglycerol increase was lower after breakfast than after lunch (20 +/- 18% and 42 +/- 40%, respectively; P < 0.04). Insulin concentrations were higher in PI-treated than in NNRTI-treated patients [22.6 (13.1-29.8) and 11.8 (7.1-19.1) microU/mL; P = 0.01] and increased in both groups in response to each meal, whereas glucose concentrations increased only after breakfast. CONCLUSIONS: Despite baseline differences, incremental triacylglycerol and insulin responses to a physiologic caloric load among HIV-positive patients were not significantly affected by differences in the type of antiretroviral therapy. Copyright © 2005 American Society for Clinical Nutrition [ABSTRACT FROM AUTHOR]

Background: Little information is available about HDL subpopulations during dietary changes. Objective: The objective was to investigate the effect of reductions in total and saturated fat intakes on HDL subpopulations. Design: Multiracial, young and elderly men and women (n = 103) participating in the double-blind, randomized DELTA (Dietary Effects on Lipoproteins and Thrombogenic Activities) Study consumed 3 different diets, each for 8 wk: an average American diet (AAD: 34.3% total fat, 15.0% saturated fat), the American Heart Association Step I diet (28.6% total fat, 9.0% saturated fat), and a diet low in saturated fat (25.3% total fat, 6.1% saturated fat). Results: HDL2-cholesterol concentrations, by differential precipitation, decreased (P < 0.001) in a stepwise fashion after the reduction of total and saturated fat: 0.58 +/= 0.21, 0.53 +/= 0.19, and 0.48 +/= 0.18 mmol/L with the AAD, Step I, and low-fat diets, respectively. HDL3 cholesterol decreased (P < 0.01) less: 0.76 +/= 0.13, 0.73 +/= 0.12, and 0.72 +/= 0.11 mmol/L with the AAD, Step I, and low-fat diets, respectively. As measured by nondenaturing gradient gel electrophoresis, the larger-size HDL2b subpopulation decreased with the reduction in dietary fat, and a corresponding relative increase was seen for the smaller-sized HDL3a, 36, and 3c subpopulations (P < 0.01). HDL2-cholesterol concentrations correlated negatively with serum triacylglycerol concentrations on all 3 diets: r = -0.46, -0.37, and -0.45 with the AAD, Step I, and low-fat diets, respectively (P < 0.0001). A similar negative correlation was seen for HDL2b, whereas HDL3a. 36, and 3c correlated positively with triacylglycerol concentrations. Diet-induced changes in serum triacylglycerol were negatively correlated with changes in HDL2 and HDL2b cholesterol. Conclusions: A reduction in dietary total and saturated fat decreased both large (HDL2 and HDL2b) and small, dense HDL subpopulations, although decreases in HDL2 and HDL2b were most pronounced. Copyright (c) 1999 American Society for Clinical Nutrition [ABSTRACT FROM AUTHOR]