Abstract

A large inter-individual variability in the plasma triglyceride (TG) response to an omega-3 polyunsaturated fatty acid (n-3 PUFA) supplementation has been observed. The objective was to examine gene-diet interaction effects on the plasma TG response after a fish oil supplementation, between single-nucleotide polymorphisms (SNPs) within genes involved in fatty acid β-oxidation and dietary fat intakes. Two hundred and eight (208) participants were recruited in the greater Quebec City area. The participants completed a six-week fish oil supplementation (5 g fish oil/day: 1.9–2.2 g EPA and 1.1 g DHA). Dietary fat intakes were measured using three-day food records. SNPs within RXRA, CPT1A, ACADVL, ACAA2, ABCD2, ACOX1 and ACAA1 genes were genotyped using TAQMAN methodology. Gene-diet interaction effects on the plasma TG response were observed for SNPs within RXRA (rs11185660, rs10881576 and rs12339187) and ACOX1 (rs17583163) genes. For rs11185660, fold changes in RXRA gene expression levels were different depending on SFA intakes for homozygotes T/T. Gene-diet interaction effects of SNPs within genes involved in fatty acid β-oxidation and dietary fat intakes may be important in understanding the inter-individual variability in plasma TG levels and in the plasma TG response to a fish oil supplementation.

Highlights

  • Plasma triglyceride (TG) level is an important risk factor for cardiovascular disease [1]

  • Fabbrini et al [8] have observed that very-low-density lipoprotein (VLDL) TG secretion was almost doubled among obese individuals with high intrahepatic TG levels

  • The objective of this study is to examine the effects of single-nucleotide polymorphisms (SNPs) within retinoid X receptor alpha (RXRA), carnitine palmitoyltransferase 1A (CPT1A), ACADVL, acyltransferase 2 (ACAA2), ABCD2, acyl-CoA oxidase 1 (ACOX1) and acyltransferase 1 (ACAA1) genes, dietary fat intakes and gene-diet interaction effects on the plasma

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Summary

Introduction

Plasma triglyceride (TG) level is an important risk factor for cardiovascular disease [1]. Twin studies have revealed that plasma TG levels are highly heritable (19%–72%) with additive genetic effects accounting for around 40% of the variability observed [2,3]. Proportions of macronutrient intake have an impact on plasma TG levels. Polyunsaturated fats (PUFA), especially n-3 PUFA, have been reported to have a beneficial impact on plasma TG levels [4,5]. At the opposite, saturated fat (SFA) intakes seem to increase intrahepatic TG levels and plasma TG levels [6,7]. Fabbrini et al [8] have observed that very-low-density lipoprotein (VLDL) TG secretion was almost doubled among obese individuals with high intrahepatic TG levels

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