Hubacek J A, Peasey A, Kubinova R, Pikhart H, Bobak M
Centre for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
Department of Epidemiology and Public Health, University College London, London, 1-19 Torrington Place, London WC1E 6BT, UK.
Nutr Metab Cardiovasc Dis. 2014 Mar;24(3):243-7. doi: 10.1016/j.numecd.2013.08.008. Epub 2013 Oct 9.
Several smaller studies reported interactions between dietary factors and apolipoprotein A5 (APOA5) gene polymorphisms in determination of plasma lipids. We tested interactions between APOA5 haplotypes and dietary intake in determination of plasma triglycerides (TG) and other lipids.
Participants (5487 males and females aged 45-69) were classified according to the number (0, 1, 2+) of minor APOA5 alleles (using T-1131 > C; rs662799 and Ser19 > Trp; rs3135506 polymorphisms) and into three groups of low (bottom 25%), medium (26th-75th percentile) and high (top 25%) of intake of total energy and total, saturated and polyunsaturated fats, assessed by food frequency questionnaire. The age-sex adjusted geometric means of plasma TG increased with the number of minor alleles, from 1.57 (standard error 0.01), to 1.79 (0.02) to 2.29 (0.10) mmol/L (p < 0.00001) but TG did not differ between groups with low, medium and high total energy intake (p = 0.251). TG concentrations were highest in subjects with the combination of 2+ minor alleles and the highest energy intake (mean 2.59 [0.19], compared with 1.62 [0.03] in subjects with lowest energy intake and no minor allele) but the interaction between energy intake and APOA5 haplotypes was not statistically significant (p = 0.186). Analogous analyses with total, saturated and polyunsaturated fat intake yielded similar nonsignificant results. Effects of APOA5 and dietary intakes on total and HDL cholesterol were weaker and no interactions were significant.
In this Slavic Caucasian population sample, we did not detect the hypothesized interaction between common SNPs within the APOA5 gene and diet in determination of blood lipids.
多项规模较小的研究报道了饮食因素与载脂蛋白A5(APOA5)基因多态性在血浆脂质测定中的相互作用。我们测试了APOA5单倍型与饮食摄入在血浆甘油三酯(TG)及其他脂质测定中的相互作用。
参与者(5487名年龄在45 - 69岁的男性和女性)根据次要APOA5等位基因的数量(0、1、2 + ,使用T - 1131 > C;rs662799和Ser19 > Trp;rs3135506多态性)进行分类,并根据通过食物频率问卷评估的总能量、总脂肪、饱和脂肪和多不饱和脂肪摄入量分为低(最低25%)、中(第26 - 75百分位数)、高(最高25%)三组。血浆TG的年龄 - 性别校正几何均值随次要等位基因数量增加而升高,从1.57(标准误0.01)mmol/L升至1.79(0.02)mmol/L再到2.29(0.10)mmol/L(p < 0.00001),但总能量摄入低、中、高组之间的TG无差异(p = 0.251)。在次要等位基因数量为2 + 且能量摄入最高的受试者中,TG浓度最高(均值2.59 [0.19]),而能量摄入最低且无次要等位基因的受试者中TG浓度为1.62 [0.03],但能量摄入与APOA5单倍型之间的相互作用无统计学意义(p = 0.186)。对总脂肪、饱和脂肪和多不饱和脂肪摄入量进行的类似分析得出了类似的无显著意义的结果。APOA5和饮食摄入对总胆固醇和高密度脂蛋白胆固醇的影响较弱,且无显著的相互作用。
在这个斯拉夫白种人群样本中,我们未检测到APOA5基因内常见单核苷酸多态性与饮食在血脂测定中的假定相互作用。