FADS1 Genetic Variability Interacts with Dietary α-Linolenic Acid Intake to Affect Serum Non-HDL-Cholesterol Concentrations in European Adolescents
FADS1 Genetic Variability Interacts with Dietary α-Linolenic Acid Intake to Affect Serum Non-HDL-Cholesterol Concentrations in European Adolescents
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DOI：
10.3945/jn.111.140392
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发表时间：
2011-07-01
影响因子：
4.2
通讯作者：
Dallongeville, Jean
中科院分区：
文献类型：
--
作者：
Dumont, Julie;Huybrechts, Inge;Dallongeville, Jean
PUFA生物合成中的两个限速酶，Delta 5-和Delta 6-去饱和酶，分别由FADS1和FADS2基因编码。FADS1-FADS2基因簇的遗传变异与血浆PUFA、HDL-和ldl -胆固醇以及TG浓度的变化有关。然而，对于膳食多聚脂肪酸摄入是否会调节这些关联，尤其是在青少年中，我们知之甚少。我们评估了青少年饮食中的亚油酸（LA）或a-亚麻酸（ALA）是否调节了FADS1 rs174546多态性与PUFA、其他脂质和脂蛋白浓度之间的关系。研究人员对来自HELENA研究的573名欧洲青少年的膳食LA和ALA摄入量、FADS1 rs174546基因型、血清磷脂中PUFA水平以及血清TG、胆固醇和脂蛋白浓度进行了测定。根据饲粮中L4 （9.4 g/d）和ALA （1.4 g/d）的中位数摄入量对样品进行分层。FADS1 rs174546与PUFA、TG、胆固醇和脂蛋白浓度之间的相关性不受膳食LA摄入量的影响（所有p相互作用均为0.05）。同样，FADS1 rs174546多态性与ALA或EPA的血清磷脂浓度之间的关联不受膳食ALA摄入量的影响（p互作均为0.05）。相比之下，rs174546次要等位基因在高ala摄入组与较低的总胆固醇浓度（优势模型下P = 0.01）和非高密度脂蛋白胆固醇浓度（优势模型下P = 0.02）相关，而在低ala摄入组与较低的总胆固醇浓度相关（P互作= 0.01）。这些结果表明，饮食中ALA的摄入调节了年轻时FADS1 rs174546与血清总胆固醇和非hdl -胆固醇浓度之间的关系。中国生物医学工程学报，21(3):444 - 444,2011。
Two rate-limiting enzymes in PUFA biosynthesis, Delta 5- and Delta 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 L4 (9.4 g/d) and ALA (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. J. Nutr. 141: 1247-1253, 2011.