Effects of peroxisome proliferator-activated receptors, dietary fat intakes and gene-diet interactions on peak particle diameters of low-density lipoproteins.

J Nutrigenet Nutrigenomics

Institute of Nutraceuticals and Functional Foods, Department of Food Science and Nutrition, Faculty of Nursing, Laval University, Québec, Canada.

Published: September 2011

Unlabelled: 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 PPARα L162V (rs1800206), PPARγ P12A (rs1801282) and PPARδ -87T→C (rs2016520) were determined by PCR-RFLP.

Results: 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).

Conclusions: These results stress that dietary factors should be included in studies determining the effect of different polymorphisms on CVD risk factors.

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http://dx.doi.org/10.1159/000324531DOI Listing

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