Bouchard-Mercier Annie, Godin Gaston, Lamarche Benoît, Pérusse Louis, Vohl Marie-Claude
Institute of Nutraceuticals and Functional Foods, Department of Food Science and Nutrition, Faculty of Nursing, Laval University, Québec, Canada.
J Nutrigenet Nutrigenomics. 2011;4(1):36-48. doi: 10.1159/000324531. Epub 2011 Apr 11.
The risk of cardiovascular diseases (CVDs) is modulated by gene-diet interactions. The objective of this study was to examine whether gene-diet interactions affect peak particle diameters (PPD) of low-density lipoprotein (LDL).
The study included 674 participants. A food frequency questionnaire was administered to obtain dietary information. LDL-PPD was determined by non-denaturing 2-16% polyacrylamide gradient gel electrophoresis. Peroxisome proliferator-activated receptor (PPAR) gene polymorphisms PPARα L162V (rs1800206), PPARγ P12A (rs1801282) and PPARδ -87T→C (rs2016520) were determined by PCR-RFLP.
Among carriers of thePPARα L162V polymorphism, gene-diet interaction effects on LDL-PPD were observed with saturated fat (p=0.0005) and total dietary fat (p=0.006). Among PPARα V162 carriers, subjects with higher saturated fat intakes had smaller LDL-PPD than those with lower intakes (254.23±2.74 vs. 256.21±2.61 Å, respectively, p=0.007). Among subjects homozygous for the PPARα L162 allele, those with higher saturated fat intakes had larger LDL-PPD than those with lower saturated fat intakes (255.86±2.66 vs. 255.05±2.65 Å, respectively, p=0.01). Gene-diet interactions were also found for PPARγ P12A polymorphism with saturated fat intake (p=0.04) and for PPARδ -87T→C with the polyunsaturated/saturated fat ratio (p=0.0013).
These results stress that dietary factors should be included in studies determining the effect of different polymorphisms on CVD risk factors.
心血管疾病（CVDs）的风险受基因 - 饮食相互作用的调节。本研究的目的是检验基因 - 饮食相互作用是否会影响低密度脂蛋白（LDL）的峰值粒径（PPD）。
该研究纳入了674名参与者。通过食物频率问卷获取饮食信息。LDL - PPD通过非变性2 - 16%聚丙烯酰胺梯度凝胶电泳测定。过氧化物酶体增殖物激活受体（PPAR）基因多态性PPARα L162V（rs1800206）、PPARγ P12A（rs1801282）和PPARδ - 87T→C（rs2016520）通过聚合酶链反应 - 限制性片段长度多态性（PCR - RFLP）测定。
在PPARα L162V多态性的携带者中，观察到饱和脂肪（p = 0.0005）和总膳食脂肪（p = 0.006）对LDL - PPD存在基因 - 饮食相互作用效应。在PPARα V162携带者中，饱和脂肪摄入量较高的受试者的LDL - PPD比摄入量较低的受试者小（分别为254.23±2.74 Å和256.21±2.61 Å，p = 0.007）。在PPARα L162等位基因纯合的受试者中，饱和脂肪摄入量较高的受试者的LDL - PPD比饱和脂肪摄入量较低的受试者大（分别为255.86±2.66 Å和255.05±2.65 Å，p = 0.01）。还发现PPARγ P12A多态性与饱和脂肪摄入量之间存在基因 - 饮食相互作用（p = 0.04），以及PPARδ - 87T→C与多不饱和/饱和脂肪比率之间存在基因 - 饮食相互作用（p = 0.0013）。
这些结果强调，在确定不同多态性对CVD危险因素影响的研究中应纳入饮食因素。
