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Garenc, Christophe

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CHU de Québec-Université Laval. Centre de recherche
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  • Publication
    Accès libre
    Omega-3 fatty acids regulate gene expression levels differently in subjects carrying the PPARα L162V polymorphism
    (Springer Nature, 2009-07-08) Garenc, Christophe; Rudkowska, Iwona; Vohl, Marie-Claude; Couture, Patrick
    Omega-3 fatty acids (FAs) are natural ligands of the peroxisome proliferator-activated receptor-α (PPARα), a nuclear receptor that modulates expression levels of genes involved in lipid metabolism. The L162V polymorphism of the PPARα gene is associated with a deteriorated metabolic profile. We postulate that subjects carrying the PPARα-V162 allele exhibit differences in the expression of PPARα and its target genes after incubation with omega-3 FAs compared with L162 homozygotes. Peripheral blood monocytes from six men carrying the PPARα-V162 allele paired for age and for body mass index with six L162 homozygotes were differentiated into macrophages and activated with eicosapentaenoic acid (EPA), docosahexaenoic acid (DHA), or mixtures of EPA:DHA. Data demonstrates that gene expression levels of PPARα and apolipoprotein AI (APOA1) were significantly lower for carriers of the PPARα-V162 allele compared to L162 homozygotes after the addition of DHA and a mixture of EPA:DHA. Additionally, lipoprotein lipase (LPL) gene expression displayed a tendency to be lower in the PPARα L162V polymorphism subgroup after the addition of a mixture of EPA:DHA. Consequently, individuals carrying the PPARα-V162 allele may demonstrate inferior improvements in their lipid profile due to alterations in gene expression rates in response to omega-3 FA supplementation.
  • Publication
    Population prevalence of APOE, APOC3 and PPAR-amutations associated to hypertriglyceridemia in French Canadians
    (Nihon Jinrui Iden Gakkai, 2004-12-01) Garenc, Christophe; Aubert, Samuel; Rousseau, François; Laroche, Jérôme; Julien, Pierre; Vohl, Marie-Claude; Bergeron, Jean
    Hypertriglyceridemia (HTG) is known as a common metabolic disorder associated with increased production, decrease catabolism and/or decreased hepatic uptake of triglyceride (TG)-rich particles. We assessed, in the Québec City population, the allele frequency and haplotype distributions of mutations in genes related to HTG, such as the apolipoprotein E (APOE) (C112R and C158R), the apolipoprotein CIII (APOC3) (C-482T and C3238G) and the peroxisome proliferator-activated receptor alpha (PPARα) (L162V) genes. A total of 938 anonymous unlinked newborns from the metropolitan Québec City area have been genotyped. Allele frequencies observed in the Québec City population differed from known frequencies determined in other Caucasian populations. The co-transmitted allele distribution between the two-marker genotypes APOE/APOC3(C3238G) and APOC3(C-482T)/PPARα(L162V) presented a weak deviation from the assumption of genetic independence. Also, we observed a non-independent distribution of the T-482/G3238 allele combinations within the APOC3 gene, suggesting strong linkage disequilibrium between the C-482T and C3238G polymorphisms. Moreover, comparisons of allele frequencies observed in the population of Québec City to those obtained in other Caucasian populations suggested that the population of Québec City may be at a lower risk of developing HTG due to APOE, APOC3 and PPARα genetic variants. However, the strong linkage disequilibrium and the two-marker genotype distributions observed in the APOC3 gene suggest that these two variants may functionally interact in the Québec City population.