Department of Nutritional Sciences, University of Surrey, Guildford GU2 7WG, UK.
Medical Research Council Human Nutrition Research, Elsie Widdowson Laboratory, Cambridge CB1 9NL, UK.
Nutrients. 2018 Oct 17;10(10):1524. doi: 10.3390/nu10101524.
We examined the impact of APOE genotype on plasma lipids and glucose in a secondary analysis of data from a five-arm, randomised controlled, parallel dietary intervention trial ('RISCK' study), to investigate the impact of replacing saturated fatty acids (SFA) with either monounsaturated fat (MUFA) or carbohydrate of high or low glycaemic index (GI) on CVD risk factors and insulin sensitivity. We tested the impact of APOE genotype (carriage of E2 and E4 alleles versus E3/E3), determined retrospectively, on plasma lipids, lipoproteins and glucose homeostasis at baseline ( = 469), and on the change in these variables after 24 weeks of dietary intervention ( = 389). At baseline, carriers of E2 ( = 70), E4 ( = 125) and E3/E3 ( = 274) expressed marked differences in total plasma cholesterol (TC, = 0.001), low density lipoprotein cholesterol (LDL-C, < 0.0001), apolipoprotein B (apo B, < 0.0001) and total to high density lipoprotein cholesterol ratio (TC:HDL-C, = 0.002), with plasma concentrations decreasing in the order E4 > E3/E3 > E2. Following intervention, there was evidence of a significant diet x genotype interaction with significantly greater decreases in TC ( = 0.02) and apo B ( = 0.006) among carriers of E4 when SFA was replaced with low GI carbohydrate on a lower fat diet (TC -0.28 mmol/L = 0.03; apo B -0.1 g/L = 0.02), and a relative increase in TC (in comparison to E3/E3) when SFA was replaced with MUFA and high GI carbohydrates (TC 0.3 mmol/L, = 0.03). Among carriers of E2 (compared with E3/E3) there was an increase in triacylglycerol (TAG) when SFA was replaced with MUFA and low GI carbohydrates 0.46 mmol/L = 0.001). There were no significant interactions between APOE genotype and diet for changes in indices of glucose homeostasis. In conclusion, variations in APOE genotype led to differential effects on the lipid response to the replacement of SFA with MUFA and low GI carbohydrates.
我们在一项五臂随机对照平行饮食干预试验（“RISCK”研究）的数据的二次分析中研究了 APOE 基因型对血浆脂质和葡萄糖的影响，以研究用单不饱和脂肪（MUFA）或高或低血糖指数（GI）碳水化合物替代饱和脂肪酸（SFA）对 CVD 风险因素和胰岛素敏感性的影响。我们测试了 APOE 基因型（携带 E2 和 E4 等位基因与 E3/E3）的影响，这是通过回顾性确定的，对基线时的血浆脂质、脂蛋白和葡萄糖稳态的影响（=469），以及对 24 周饮食干预后这些变量变化的影响（=389）。在基线时，E2 携带者（=70）、E4 携带者（=125）和 E3/E3 携带者（=274）在总血浆胆固醇（TC，=0.001）、低密度脂蛋白胆固醇（LDL-C，<0.0001）、载脂蛋白 B（apo B，<0.0001）和总到高密度脂蛋白胆固醇比值（TC:HDL-C，=0.002）方面存在明显差异，血浆浓度按 E4>E3/E3>E2 的顺序降低。干预后，有证据表明饮食与基因型存在显著的相互作用，当 SFA 被低 GI 碳水化合物取代时，E4 携带者的 TC（=0.02）和 apo B（=0.006）明显下降（TC-0.28mmol/L，=0.03；apo B-0.1g/L，=0.02），而当 SFA 被 MUFA 和高 GI 碳水化合物取代时，E4 携带者的 TC 相对增加（与 E3/E3 相比）（TC0.3mmol/L，=0.03）。与 E3/E3 相比，E2 携带者（E2）的三酰甘油（TAG）在 SFA 被 MUFA 和低 GI 碳水化合物取代时增加（0.46mmol/L，=0.001）。APOE 基因型与饮食之间在葡萄糖稳态变化方面没有显著的相互作用。总之，APOE 基因型的变化导致了用 MUFA 和低 GI 碳水化合物替代 SFA 对血脂反应的不同影响。
