期刊
CURRENT OPINION IN CLINICAL NUTRITION AND METABOLIC CARE
卷 19, 期 2, 页码 103-110出版社
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/MCO.0000000000000254
关键词
desaturase; elongase; long-chain polyunsaturated fatty acids; single nucleotide polymorphisms
资金
- NIH from the National Center for Complementary and Integrative Health (NCCIH) [R01 AT007003]
- Office of Dietary Supplements (ODS)
Purpose of reviewEndogenous synthesis of the long-chain polyunsaturated fatty acids (LCPUFAs) is mediated by the fatty acid desaturase (FADS) gene cluster (11q12-13.1) and elongation of very long-chain fatty acids 2 (ELOVL2) (6p24.2) and ELOVL5 (6p12.1). Although older biochemical work identified the product of one gene, FADS2, rate limiting for LCPUFA synthesis, recent studies suggest that polymorphisms in any of these genes can limit accumulation of product LCPUFA.Recent findingsGenome-wide association study (GWAS) of Greenland Inuit shows strong adaptation signals within FADS gene cluster, attributed to high omega-3 fatty acid intake, while GWAS found ELOVL2 associated with sleep duration, age and DNA methylation. ELOVL5 coding mutations cause spinocerebellar ataxia 38, and epigenetic marks were associated with depression and suicide risk. Two sterol response element binding sites were found on ELOVL5, a SREBP-1c target gene. Minor allele carriers of a 3 single nucleotide polymorphism (SNP) haplotype in ELOVL2 have decreased 22:6n-3 levels. Unequivocal molecular evidence shows mammalian FADS2 catalyzes direct 4-desaturation to yield 22:6n-3 and 22:5n-6. An SNP near FADS1 influences the levels of 5-lipoxygenase products and epigenetic alteration.SummaryGenetic polymorphisms within FADS and ELOVL can limit LCPUFA product accumulation at any step of the biosynthetic pathway.
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