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Apolipoprotein E gene promoter –219GT polymorphism increases LDL-cholesterol concentrations and susceptibility to oxidation in response to a diet rich in saturated fat^1,2,3

¹ From the Lipids and Atherosclerosis Research Unit, Reina Sofía University Hospital, Córdoba, Spain

Background: The apolipoprotein E (APOE) gene promoter polymorphism (–219GT) has been associated with increased risk of myocardial infarction, premature coronary artery disease, and decreased plasma apolipoprotein E concentrations.

Objective: We aimed to determine in healthy subjects whether this polymorphism modifies the susceptibility of LDL to oxidation and the lipid response to the content and quality of dietary fat.

Design: Fifty-five healthy men with the APOE3/E3 genotype (7 GG, 38 GT, and 10 TT) completed 3 dietary periods, each lasting 4 wk. The first was a saturated fatty acid (SFA)-rich diet [38% fat—20% SFA and 12% monounsaturated fatty acid (MUFA)—and 47% carbohydrates (CHO)], which was followed by a CHO-rich diet (30% fat—<10% SFA and 12% MUFA—and 55% CHO) or a MUFA-rich diet (38% fat—<10% SFA and 22% MUFA—and 47% CHO) in a randomized crossover design. At the end of each dietary period, LDL oxidation susceptibility, lipids, and lipoproteins were measured.

Results: Compared with carriers of the G allele, TT subjects had a significantly (P < 0.05) shorter lag time after the SFA diet. The replacement of the SFA diet by the CHO or MUFA diet induced a greater increase (P < 0.05) in lag time in the TT subjects than in the GG or GT subjects. Carriers of the T allele had higher LDL-cholesterol (P < 0.05) and apolipoprotein B (P < 0.05) plasma concentrations after the SFA diet than did GG subjects. Compared with GG subjects, carriers of the T allele had a significantly (P < 0.05) greater decrease in LDL cholesterol and apolipoprotein B when they changed from the SFA to the CHO diet.

Conclusion: The –219GT polymorphism may partially explain differences in individual responses to diet.

Key Words: Apolipoprotein E gene promoter polymorphism • –219GT • APOE • dietary intervention • LDL oxidation • LDL cholesterol • cardiovascular disease risk

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