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Cardiometabolic risk factors are influenced by Stearoyl‐CoA Desaturase‐1 (SCD1) polymorphisms and n‐3 polyunsaturated fatty acids supplementation
Author(s) -
Rudkowska Iwona,
Julien Pierre,
Couture Patrick,
Lemieux Simone,
Vohl MarieClaude
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.640.10
Subject(s) - polyunsaturated fatty acid , single nucleotide polymorphism , fish oil , snp , stearoyl coa desaturase , endocrinology , medicine , chemistry , biology , food science , genotype , gene , biochemistry , fatty acid , fish <actinopterygii> , gene expression , fishery
Polymorphisms (SNPs) in the stearoyl‐CoA desaturase‐1 ( SCD1 ) gene may play a role in the development of the metabolic syndrome. Objective To determine if SCD1 gene SNPs are associated with cardiometabolic risk factors prior and after n ‐3 polyunsaturated fatty acids (PUFA) supplementation. Methods 210 subjects completed a 2‐wk run‐in period followed by 6‐wk supplementation with 5g of fish oil (1.9g EPA and 1.1g DHA). Risk factors were measured pre‐ and post‐ supplementation. FA composition of plasma phospholipids was analyzed by gas chromatography and the desaturase indices were calculated SCD16 (16:1n‐7/16:0) and SCD18 (18:1n‐9/18:0). Genotyping of 8 SNPs of the SCD1 gene was performed. Results N ‐3 PUFA supplementation decreased plasma triglycerides (TG), SCD16 and SCD18 ratios with an increased plasma glucose levels. In repeated measures analysis of variance, where the effects of interest were SNP, supplementation and interaction between the SNP*supplementation on cardiometabolic risk factors, SNPs in SCD1 modified: TG ( rs508384 ), interleukin‐6 (rs3071), C‐reactive protein (rs3829160) and SCD18 ratio (rs2234970). Interaction effects were observed for plasma glucose ( rs508384 ) and insulin levels ( rs508384 and rs3829160). Conclusion Cardiometabolic risk factors are modulated by genetic variations in the SCD1 gene alone or in combination with n ‐3 PUFA supplementation. Funding: CIHR .