FADS1 Genetic Variability Interacts with Dietary a-Linolenic Acid Intake to Affect Serum Non-HDL–Cholesterol Concentrations in European Adolescents  

Oleh:

Dumont, Julie ; Huybrechts, Inge ; Spinneker, Andre ; Gottrand, Frederic

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: JN: The Journal of Nutrition vol. 141 no. 07 (Jul. 2011), page 1247-1253 .
Topik: Biochemical; Molecular; Genetic Mechanisms

Ketersediaan

Perpustakaan FK Nomor Panggil: J42.K.2011.02 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Isi artikel

Two rate-limiting enzymes in PUFA biosynthesis, ?5- and ?6-desaturases, are encoded by the FADS1 and FADS2 genes, respectively. Genetic variants in the FADS1-FADS2 gene cluster are associated with changes in plasma concentrations of PUFA, HDL- and LDL-cholesterol, and TG. However, little is known about whether dietary PUFA intake modulates these associations, especially in adolescents. We assessed whether dietary linoleic acid (LA) or a-linolenic acid (ALA) modulate the association between the FADS1 rs174546 polymorphism and concentrations of PUFA, other lipids, and lipoproteins in adolescents. Dietary intakes of LA and ALA, FADS1 rs174546 genotypes, PUFA levels in serum phospholipids, and serum concentrations of TG, cholesterol, and lipoproteins were determined in 573 European adolescents from the HELENA study. The sample was stratified according to the median dietary LA (=9.4 and >9.4 g/d) and ALA (=1.4 and >1.4 g/d) intakes. The associations between FADS1 rs174546 and concentrations of PUFA, TG, cholesterol, and lipoproteins were not affected by dietary LA intake (all P-interaction > 0.05). Similarly, the association between the FADS1 rs174546 polymorphism and serum phospholipid concentrations of ALA or EPA was not modified by dietary ALA intake (all P-interaction > 0.05). In contrast, the rs174546 minor allele was associated with lower total cholesterol concentrations (P = 0.01 under the dominant model) and non-HDL–cholesterol concentrations (P = 0.02 under the dominant model) in the high-ALA–intake group but not in the low-ALA–intake group (P-interaction = 0.01). These results suggest that dietary ALA intake modulates the association between FADS1 rs174546 and serum total and non-HDL–cholesterol concentrations at a young age.

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