Genes, fat intake, and cardiovascular disease risk factors in the Quebec family study

被引:19
作者
Robitaille, Julie
Perusse, Louis
Bouchard, Claude
Vohl, Marie-Claude
机构
[1] Univ Quebec, Ctr Hosp Univ Laval Pavilion, Lipid Res Ctr, Ste Foy, PQ, Canada
[2] Univ Laval, Dept Food Sci & Nutr, Quebec City, PQ G1K 7P4, Canada
[3] Univ Laval, Dept Social & Prevent Med, Div Kinesiol, Quebec City, PQ G1K 7P4, Canada
[4] Pennington Biomed Res Ctr, Baton Rouge, LA USA
关键词
abdominal obesity; dietary fat intake; hypertension; hypertriglyceridemia; hyperglycemia;
D O I
10.1038/oby.2007.277
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective: The aim of this study was to assess gene-diet interaction effects on cardiovascular disease (CVD) risk factors (waist circumference, plasma triacylglycerol, high-density lipoprotein-cholesterol and fasting glucose concentrations, and diastolic and systolic blood pressure) in the Quebec Family Study cohort. Design: Sixty-four polymorphisms from 45 candidate genes were studied in 645 subjects. Dietary fat intake was obtained from a 3-day weighted food record. Results: We observed 18 significant interactions at a p value <= 0.01. Among them, the Pro12A1a polymorphism in peroxisome proliferator-activated receptor gamma, alone or in interaction with fat intake, significantly modulated waist circumference (p = 0.0005 for both effects). Additionally, the apolipoprotein E genotype in interaction with fat intake was significantly associated with diastolic and systolic blood pressure (p = 0.01 and p = 0.001, respectively). The ghrelin Leu72Met polymorphism also interacted with dietary fat in its relation to waist circumference and triacylglycerol concentrations (p = 0.0004 and p = 0.005). Discussion: These results suggest that several alleles at candidate genes interact with dietary fat intake to modulate well-known CVD risk factors. The identification of gene-diet interaction effects is likely to provide useful information concerning the etiology of CVD.
引用
收藏
页码:2336 / 2347
页数:12
相关论文
共 97 条
[1]  
ADKINS S, 1993, AM J HUM GENET, V52, P598
[2]   AMINO-ACID POLYMORPHISMS OF INSULIN-RECEPTOR SUBSTRATE-1 IN NON-INSULIN-DEPENDENT DIABETES-MELLITUS [J].
ALMIND, K ;
BJORBAEK, C ;
VESTERGAARD, H ;
HANSEN, T ;
ECHWALD, S ;
PEDERSEN, O .
LANCET, 1993, 342 (8875) :828-832
[3]   The common PPARγ Pro12Ala polymorphism is associated with decreased risk of type 2 diabetes [J].
Altshuler, D ;
Hirschhorn, JN ;
Klannemark, M ;
Lindgren, CM ;
Vohl, MC ;
Nemesh, J ;
Lane, CR ;
Schaffner, SF ;
Bolk, S ;
Brewer, C ;
Tuomi, T ;
Gaudet, D ;
Hudson, TJ ;
Daly, M ;
Groop, L ;
Lander, ES .
NATURE GENETICS, 2000, 26 (01) :76-80
[4]  
[Anonymous], 1990, Q REV BIOL
[5]  
[Anonymous], P 5 BERK S MATH STAT
[6]   Factors of insulin resistance syndrome-related phenotypes are linked to genetic locations on chromosomes 6 and 7 in nondiabetic Mexican-Americans [J].
Arya, R ;
Blangero, J ;
Williams, K ;
Almasy, L ;
Dyer, TD ;
Leach, RJ ;
O'Connell, P ;
Stern, MP ;
Duggirala, R .
DIABETES, 2002, 51 (03) :841-847
[7]   AN AMINO-ACID SUBSTITUTION IN THE HUMAN INTESTINAL FATTY-ACID-BINDING PROTEIN IS ASSOCIATED WITH INCREASED FATTY-ACID-BINDING, INCREASED FAT OXIDATION, AND INSULIN-RESISTANCE [J].
BAIER, LJ ;
SACCHETTINI, JC ;
KNOWLER, WC ;
EADS, J ;
PAOLISSO, G ;
TATARANNI, PA ;
MOCHIZUKI, H ;
BENNETT, PH ;
BOGARDUS, C ;
PROCHAZKA, M .
JOURNAL OF CLINICAL INVESTIGATION, 1995, 95 (03) :1281-1287
[8]   Respiratory uncoupling lowers blood pressure through a leptin-dependent mechanism in genetically obese mice [J].
Bernal-Mizrachi, C ;
Weng, S ;
Li, B ;
Nolte, LA ;
Feng, C ;
Coleman, T ;
Holloszy, JO ;
Semenkovich, CF .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2002, 22 (06) :961-968
[9]   Genome-wide linkage scan reveals multiple susceptibility loci influencing lipid and lipoprotein levels in the Quebec Family Study [J].
Bossé, Y ;
Chagnon, YC ;
Després, CJP ;
Rice, T ;
Rao, DC ;
Bouchard, C ;
Pérusse, L ;
Vohl, MC .
JOURNAL OF LIPID RESEARCH, 2004, 45 (03) :419-426
[10]  
BOUCHARD C, 1996, MOL GENETIC ASPECTS