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心脏代谢风险因素受 Stearoyl-CoA 脱饱和酶(SCD)-1 基因多态性和 n-3 多不饱和脂肪酸补充的影响。

Cardiometabolic risk factors are influenced by Stearoyl-CoA Desaturase (SCD) -1 gene polymorphisms and n-3 polyunsaturated fatty acid supplementation.

机构信息

Institute of Nutrition and Functional Foods (INAF), Laval University, Quebec, Canada; Department of Endocrinology and Nephrology, CHU de Québec Research Center, Quebec, Canada.

出版信息

Mol Nutr Food Res. 2014 May;58(5):1079-86. doi: 10.1002/mnfr.201300426. Epub 2013 Dec 23.

DOI:10.1002/mnfr.201300426
PMID:24375980
Abstract

SCOPE

To determine if single nucleotide polymorphisms (SNPs) in stearoyl-CoA desaturase (SCD)-1 gene that encodes a key enzyme for fatty acid metabolism are associated with the response of cardiometabolic risk factors to n-3 PUFA supplementation.

METHODS AND RESULTS

Two hundred and ten subjects completed a 2-week run-in period followed by 6-week supplementation with 5 g of fish oil (1.9-2.2 g eicosapentaenoic acid and 1.1 g docosahexaenoic acid). Risk factors were measured pre and post n-3 supplementation. Fatty acid composition of plasma phospholipids was analyzed by GC and the desaturase indices SCD16 (16:1n-7/16:0) and SCD18 (18:1n-9/18:0) were calculated. Genotyping of eight SNPs of the SCD1 gene was performed. N-3 PUFA supplementation decreased plasma triglycerides, as well as SCD16 and SCD18 indices, but increased fasting plasma glucose concentrations. SNPs in SCD1-modified cardiometabolic risk factors pre and post n-3 PUFA supplementation: triglyceride (rs508384, p = 0.0086), IL6 (rs3071, p = 0.0485), C-reactive protein (rs3829160, p = 0.0489), and SCD18 indices (rs2234970, p = 0.0337). A significant interaction effect between the SNP and n-3 PUFA supplementation was also observed for fasting plasma glucose levels (rs508384, p = 0.0262).

CONCLUSION

These results suggest that cardiometabolic risk factors are modulated by genetic variations in the SCD1 gene alone or in combination with n-3 PUFA supplementation.

摘要

范围

确定编码脂肪酸代谢关键酶的硬脂酰辅酶 A 去饱和酶 (SCD)-1 基因中的单核苷酸多态性 (SNP) 是否与 n-3PUFA 补充对心脏代谢风险因素的反应有关。

方法和结果

210 名受试者完成了为期 2 周的导入期,随后进行了 6 周的鱼油补充,剂量为 5 克(1.9-2.2 克二十碳五烯酸和 1.1 克二十二碳六烯酸)。在 n-3 补充前后测量风险因素。通过 GC 分析血浆磷脂中的脂肪酸组成,并计算去饱和酶指数 SCD16(16:1n-7/16:0)和 SCD18(18:1n-9/18:0)。对 SCD1 基因的 8 个 SNP 进行基因分型。n-3PUFA 补充降低了血浆甘油三酯以及 SCD16 和 SCD18 指数,但增加了空腹血糖浓度。SCD1 基因中的 SNP 改变了 n-3PUFA 补充前后的心脏代谢风险因素:甘油三酯(rs508384,p=0.0086)、白细胞介素 6(rs3071,p=0.0485)、C 反应蛋白(rs3829160,p=0.0489)和 SCD18 指数(rs2234970,p=0.0337)。还观察到 SNP 和 n-3PUFA 补充之间存在显著的交互作用,空腹血糖水平也受到影响(rs508384,p=0.0262)。

结论

这些结果表明,心脏代谢风险因素受到 SCD1 基因中遗传变异的单独或与 n-3PUFA 补充的联合调节。

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