Dang Thuy Mai, Conway Valérie, Plourde Mélanie
Department of Physiology, Université de Sherbrooke, Sherbrooke, Canada; Research Center on Aging, Health and Social Sciences Center, University Institute of Geriatrics of Sherbrooke, Sherbrooke, Canada.
Research Center on Aging, Health and Social Sciences Center, University Institute of Geriatrics of Sherbrooke, Sherbrooke, Canada; Department of Medicine, Université de Sherbrooke, Sherbrooke, Canada.
Nutrition. 2015 Jun;31(6):807-12. doi: 10.1016/j.nut.2014.11.019. Epub 2014 Dec 24.
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.
载脂蛋白E的ε4等位基因携带者（E4+）的ω-3多不饱和脂肪酸（ω-3 PUFA）代谢似乎受到破坏。本研究的目的是调查在补充ω-3多不饱和脂肪酸前后，高密度脂蛋白和低密度脂蛋白中ω-3多不饱和脂肪酸的分布是否依赖于载脂蛋白E基因型。
招募了80名年龄在20至35岁之间的参与者，补充900毫克二十碳五烯酸加680毫克二十二碳六烯酸，为期4周。在4周的干预期间，采集血样，使用蔗糖梯度超速离心法获得高密度脂蛋白和低密度脂蛋白颗粒。通过气相色谱法分析高密度脂蛋白和低密度脂蛋白组分的脂肪酸谱。
两组载脂蛋白E组（E4+，n = 10；E4-，n = 70）参与者的基线人体测量特征无显著差异。基线时，E4+受试者的低密度脂蛋白中ω-6/ω-3多不饱和脂肪酸比值比E4-受试者高17%。在第4周时，E4+受试者的低密度脂蛋白中ω-6/ω-3多不饱和脂肪酸比值显著高于E4-受试者。高密度脂蛋白和低密度脂蛋白中的16:0以及高密度脂蛋白中的18:2 ω-6存在显著的基因型×时间交互作用。仅在E4-组中，补充前后高密度脂蛋白中的二十二碳六烯酸与高密度脂蛋白胆固醇水平呈正相关。
与我们的预期相反，年轻参与者高密度脂蛋白和低密度脂蛋白中的ω-3多不饱和脂肪酸含量并不依赖于载脂蛋白E异构体。然而，年轻的E4+参与者在低密度脂蛋白颗粒中的基线二十二碳六烯酸水平已经有降低的趋势，并且在补充前后低密度脂蛋白中的ω-6/ω-3多不饱和脂肪酸比值更具致动脉粥样硬化性。
