Effects of Peroxisome Proliferator-Activated Receptors, Dietary Fat Intakes and Gene-Diet Interactions on Peak Particle Diameters of Low-Density Lipoproteins

被引:23
作者
Bouchard-Mercier, Annie [1 ,2 ]
Godin, Gaston [3 ]
Lamarche, Benoit [1 ,2 ]
Perusse, Louis [1 ,4 ]
Vohl, Marie-Claude [1 ,2 ]
机构
[1] Univ Laval, Inst Nutraceut & Funct Foods, Quebec City, PQ G1K 7P4, Canada
[2] Univ Laval, Dept Food Sci & Nutr, Quebec City, PQ G1K 7P4, Canada
[3] Univ Laval, Fac Nursing, Quebec City, PQ G1K 7P4, Canada
[4] Univ Laval, Dept Social & Prevent Med, Div Kinesiol, Quebec City, PQ G1K 7P4, Canada
基金
加拿大健康研究院;
关键词
Dietary fat; Gene polymorphisms; Low-density lipoprotein; Particle diameters; Peroxisome proliferator-activated receptors; PPAR alpha; PPAR delta; PPAR gamma; CORONARY-HEART-DISEASE; GAMMA GENE; METABOLIC SYNDROME; SATURATED FAT; PPAR-ALPHA; LDL SIZE; POLYMORPHISM; ACIDS; CHOLESTEROL; RISK;
D O I
10.1159/000324531
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
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). Methods: 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 PPAR alpha L162V (rs1800206), PPAR-gamma P12A (rs1801282) and PPAR delta-87T -> C (rs2016520) were determined by PCR-RFLP. Results: Among carriers of the PPARa 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 PPAR alpha 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 A, respectively, p = 0.007). Among subjects homozygous for the PPAR alpha 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 A, respectively, p = 0.01). Gene diet interactions were also found for PPAR gamma P12A polymorphism with saturated fat intake (p = 0.04) and for PPAR delta -87T -> C with the polyunsaturated/saturated fat ratio (p = 0.0013). Conclusions: These results stress that dietary factors should be included in studies determining the effect of different polymorphisms on CVD risk factors. Copyright (C) 2011 S. Karger AG, Basel
引用
收藏
页码:36 / 48
页数:13
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