Disrupted fatty acid distribution in HDL and LDL according to apolipoprotein E allele

Omega-3 polyunsaturated fatty acid (ω-3 PUFA) metabolism seems to be disrupted in carriers of the epsilon 4 allele of apolipoprotein E (E4+). The objective of this study was to investigate whether the ω-3 PUFA distribution in the high and low density lipoproteins is APOE-genotype dependant before and after supplementation with ω-3 PUFAs.

Eighty participants, aged between 20 and 35 y old were recruited and supplemented with 900 mg of eicosapentaenoic acid plus 680 mg of docosahexaenoic acid for 4 wk. Over the 4-wk intervention, blood samples were collected and HDL and LDL particles were obtained using sucrose gradient ultracentifugation. Fatty acid profiles of the HDL and LDL fractions were performed by gas chromatography.

Baseline anthropometric characteristics of participants were not significantly different between the two APOE-groups (E4+, N = 10; E4-, N = 70). At baseline, in the LDL of E4+ subjects, the ω-6/ω-3 PUFA ratio was 17% higher than E4- subjects. At week 4, the ω-6/ω-3 PUFA ratio was significantly higher in the LDL of E4+ than E4- subjects. There was a significant genotype × time interaction for 16:0 in HDL and LDL and for 18:2 ω-6 in HDL. DHA in the HDL was positively correlated to HDL-C levels pre- and postsupplementation in E4- only.

Contrary to what we anticipated, ω-3 PUFAs content? in HDL and LDL were not APOE isoform-dependant in young participants. However, young E4+ participants already had a tendency toward lower baseline-DHA levels in LDL particles as well as a more atherogenic ω-6/ω-3 PUFA ratio in LDL pre- and post-supplementation.