Cardiometabolic risk factors are influenced by S tearoyl‐ C o A D esaturase ( SCD ) − 1 gene polymorphisms and n ‐3 polyunsaturated fatty acid supplementation

Scope To determine if single nucleotide polymorphisms ( SNP s) in stearoyl‐ C o A 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 SCD 16 (16:1n‐7/16:0) and SCD 18 (18:1n‐9/18:0) were calculated. Genotyping of eight SNP s of the SCD 1 gene was performed. N ‐3 PUFA supplementation decreased plasma triglycerides, as well as SCD 16 and SCD 18 indices, but increased fasting plasma glucose concentrations. SNP s in SCD 1 ‐modified cardiometabolic risk factors pre and post n ‐3 PUFA supplementation: triglyceride (rs508384, p = 0.0086), IL 6 (rs3071, p = 0.0485), C‐reactive protein (rs3829160, p = 0.0489), and SCD 18 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 SCD 1 gene alone or in combination with n ‐3 PUFA supplementation.