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Original Research Communication |
1 From the Unidad de Lipidos y Arteriosclerosis, Hospital Universitario Reina Sofía, Cordoba, Spain (CM, JL-M, PG, EP, PP-M, FF, JAJ-P, and FP-J), and the Lipid Metabolism Laboratory, Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging, Tufts University, Boston (JMO).
Background: There is considerable interindividual variability in the postprandial lipid response to a fat-rich meal, and genetic factors have been considered to account for some of these effects. We previously showed that the G-A mutation 5' to the apolipoprotein (apo) A-I gene was significantly associated with the LDL-cholesterol response to diet.
Objective: We evaluated whether this effect is mediated by mechanisms involving postprandial lipoprotein metabolism.
Design: Twenty-eight G/G and 23 G/A healthy male subjects, homozygotes for the apo E3 allele, were subjected to a vitamin A fat-loading test. Blood was drawn at time 0 and every hour for 11 h.
Results: There was a significant postprandial decrease in plasma cholesterol, LDL cholesterol, and apo B in G/G subjects but not in G/A subjects. A greater postprandial response in large triacylglycerol-rich lipoproteins (TRLs) and a smaller postprandial response in large TRL apo A-IV was observed in G/A than in G/G subjects. Retinyl palmitate in large and small TRL concentrations was similar for both genotypes. No significant genotype effects were detected for triacylglycerol concentrations in plasma, small TRL fraction, and apo A-I and HDL-cholesterol concentrations.
Conclusion: Our data suggest that the G-A mutation affects the LDL-cholesterol response to diet by mechanisms involving postprandial lipoprotein cholesterol metabolism.
Key Words: Postprandial lipemia • apolipoprotein A-I • G-A mutation • triacylglycerols • retinyl palmitate • coronary artery disease • HDL cholesterol • LDL cholesterol
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