脂肪酸去饱和酶（FADS）基因簇多态性：ω-3 多不饱和脂肪酸（PUFA）补充对血糖控制的影响。
Polymorphisms in Fatty Acid Desaturase (FADS) Gene Cluster: Effects on Glycemic Controls Following an Omega-3 Polyunsaturated Fatty Acids (PUFA) Supplementation.
机构信息
Institute of Nutrition and Functional Foods (INAF), Laval University, Quebec City, QC, G1V 0A6, Canada.
出版信息
Genes (Basel). 2013 Sep 10;4(3):485-98. doi: 10.3390/genes4030485.
UNLABELLED
Changes in desaturase activity are associated with insulin sensitivity and may be associated with type 2 diabetes mellitus (T2DM). Polymorphisms (SNPs) in the fatty acid desaturase (FADS) gene cluster have been associated with the homeostasis model assessment of insulin sensitivity (HOMA-IS) and serum fatty acid composition.
OBJECTIVE
To investigate whether common genetic variations in the FADS gene cluster influence fasting glucose (FG) and fasting insulin (FI) responses following a 6-week n-3 polyunsaturated fatty acids (PUFA) supplementation.
METHODS
210 subjects completed a 2-week run-in period followed by a 6-week supplementation with 5 g/d of fish oil (providing 1.9 g-2.2 g of EPA + 1.1 g of DHA). Genotyping of 18 SNPs of the FADS gene cluster covering 90% of all common genetic variations (minor allele frequency ≥ 0.03) was performed.
RESULTS
Carriers of the minor allele for rs482548 (FADS2) had increased plasma FG levels after the n-3 PUFA supplementation in a model adjusted for FG levels at baseline, age, sex, and BMI. A significant genotypesupplementation interaction effect on FG levels was observed for rs482548 (p = 0.008). For FI levels, a genotype effect was observed with one SNP (rs174456). For HOMA-IS, several genotypesupplementation interaction effects were observed for rs7394871, rs174602, rs174570, rs7482316 and rs482548 (p = 0.03, p = 0.01, p = 0.03, p = 0.05 and p = 0.07; respectively).
CONCLUSION
RESULTS suggest that SNPs in the FADS gene cluster may modulate plasma FG, FI and HOMA-IS levels in response to n-3 PUFA supplementation.
非标记
去饱和酶活性的变化与胰岛素敏感性有关，可能与 2 型糖尿病（T2DM）有关。脂肪酸去饱和酶（FADS）基因簇中的多态性（SNP）与胰岛素敏感的稳态模型评估（HOMA-IS）和血清脂肪酸组成有关。
目的
研究 FADS 基因簇中的常见遗传变异是否影响 6 周 n-3 多不饱和脂肪酸（PUFA）补充后的空腹血糖（FG）和空腹胰岛素（FI）反应。
方法
210 名受试者完成了 2 周的适应期，随后进行了 6 周的鱼油补充，每天 5 克（提供 1.9-2.2 克 EPA 和 1.1 克 DHA）。对 FADS 基因簇的 18 个 SNP 进行基因分型，这些 SNP 覆盖了所有常见遗传变异的 90%（次要等位基因频率≥0.03）。
结果
在调整了基线 FG 水平、年龄、性别和 BMI 的模型中，rs482548（FADS2）的次要等位基因携带者在 n-3 PUFA 补充后血浆 FG 水平升高。rs482548 观察到 FG 水平的显著基因型补充相互作用效应（p=0.008）。对于 FI 水平，一个 SNP（rs174456）观察到基因型效应。对于 HOMA-IS，rs7394871、rs174602、rs174570、rs7482316 和 rs482548 观察到几个基因型补充相互作用效应（p=0.03、p=0.01、p=0.03、p=0.05 和 p=0.07；分别）。
结论
结果表明，FADS 基因簇中的 SNP 可能调节 n-3 PUFA 补充后血浆 FG、FI 和 HOMA-IS 水平。
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