This article is about the gene, for main associated enzyme see D6D.
Fatty acid desaturase 2 (FADS2) is encoded by the FADS2gene, the associated enzyme is sometimes known as FADS2 as well.[1][2] Its main associated enzyme is Delta 6 desaturase (D6D) however the human enzyme been shown to also catalyze some delta-8 and delta-4 desaturases in spite of naming conventions.[3]
Fatty acid desaturase 2 is a member of the fatty acid desaturase (FADS) gene family. Desaturase enzymes cause desaturation of fatty acids through the introduction of double bonds between defined carbons of the fatty acyl chain. FADS family members are considered fusion products composed of an N-terminalcytochrome b5-like domain and a C-terminal multiple membrane-spanning desaturase portion, both of which are characterized by conserved histidine motifs. This gene is clustered with family members FADS1 and FADS2 at 11q12-q13.1; this cluster is thought to have arisen evolutionarily from gene duplication based on its similar exon/intron organization.[1]
It was reported the FADS2 interacts with breastfeeding such that breast-fed children with the "C" version of the gene appear about 7 intelligence quotient (IQ) points higher than those with the less common "G" version (less than this when adjusted for maternal IQ).[4][5]
An attempt to replicate this study in 5934 8 year old children failed: No relationship of the common C allele to negative effects of formula feeding was apparent, and contra to the original report, the rare GG homozygote children performed worse when formula fed than other children on formula milk.[6] A study of over 700 families recently found no evidence for either main or moderating effects of the original SNP (rs174575), nor of two additional FADS2 polymorphisms (rs1535 and rs174583), nor any effect of maternal FADS2 status on offspring IQ.[7]
↑Marquardt A, Stöhr H, White K, Weber BH (June 2000). "cDNA cloning, genomic structure, and chromosomal localization of three members of the human fatty acid desaturase family". Genomics. 66 (2): 175–83. doi:10.1006/geno.2000.6196. PMID10860662.
Lattka E, Illig T, Koletzko B, Heinrich J (2010). "Genetic variants of the FADS1 FADS2 gene cluster as related to essential fatty acid metabolism". Curr. Opin. Lipidol. 21 (1): 64–9. doi:10.1097/MOL.0b013e3283327ca8. PMID19809313.
Xie L, Innis SM (2009). "Association of fatty acid desaturase gene polymorphisms with blood lipid essential fatty acids and perinatal depression among Canadian women: a pilot study". J. Nutr. Nutr. 2 (4–5): 243–50. doi:10.1159/000255636. PMID20395685.
Kwak JH, Paik JK, Kim OY, et al. (2011). "FADS gene polymorphisms in Koreans: association with ω6 polyunsaturated fatty acids in serum phospholipids, lipid peroxides, and coronary artery disease". Atherosclerosis. 214 (1): 94–100. doi:10.1016/j.atherosclerosis.2010.10.004. PMID21040914.
Lattka E, Illig T, Heinrich J, Koletzko B (2009). "FADS gene cluster polymorphisms: important modulators of fatty acid levels and their impact on atopic diseases". J. Nutr. Nutr. 2 (3): 119–28. doi:10.1159/000235559. PMID19776639.
Lattka E, Illig T, Heinrich J, Koletzko B (2010). "Do FADS genotypes enhance our knowledge about fatty acid related phenotypes?". Clin Nutr. 29 (3): 277–87. doi:10.1016/j.clnu.2009.11.005. PMID19948371.
Koletzko B, Lattka E, Zeilinger S, et al. (2011). "Genetic variants of the fatty acid desaturase gene cluster predict amounts of red blood cell docosahexaenoic and other polyunsaturated fatty acids in pregnant women: findings from the Avon Longitudinal Study of Parents and Children". Am. J. Clin. Nutr. 93 (1): 211–9. doi:10.3945/ajcn.110.006189. PMID21106917.
Kröger J, Zietemann V, Enzenbach C, et al. (2011). "Erythrocyte membrane phospholipid fatty acids, desaturase activity, and dietary fatty acids in relation to risk of type 2 diabetes in the European Prospective Investigation into Cancer and Nutrition (EPIC)-Potsdam Study". Am. J. Clin. Nutr. 93 (1): 127–42. doi:10.3945/ajcn.110.005447. PMID20980488.
Koletzko B, Demmelmair H, Schaeffer L, et al. (2008). "Genetically determined variation in polyunsaturated fatty acid metabolism may result in different dietary requirements". Nestle Nutr Workshop Ser Pediatr Program. 62: 35–44, discussion 44-9. doi:10.1159/000146246. PMID18626191.
Zietemann V, Kröger J, Enzenbach C, Jansen E, Fritsche A, Weikert C, Boeing H, Schulze MB (December 2010). "Genetic variation of the FADS1 FADS2 gene cluster and n-6 PUFA composition in erythrocyte membranes in the European Prospective Investigation into Cancer and Nutrition-Potsdam study". Br. J. Nutr. 104 (12): 1748–59. doi:10.1017/S0007114510002916. PMID20691134.
Park MH, Kim N, Lee JY, Park HY (2011). "Genetic loci associated with lipid concentrations and cardiovascular risk factors in the Korean population". J. Med. Genet. 48 (1): 10–5. doi:10.1136/jmg.2010.081000. PMID20972250.
Lu Y, Feskens EJ, Dollé ME, Imholz S, Verschuren WM, Müller M, Boer JM (July 2010). "Dietary n-3 and n-6 polyunsaturated fatty acid intake interacts with FADS1 genetic variation to affect total and HDL-cholesterol concentrations in the Doetinchem Cohort Study". Am. J. Clin. Nutr. 92 (1): 258–65. doi:10.3945/ajcn.2009.29130. PMID20484448.
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