Linoleoyl-CoA desaturase (also Delta 6 desaturase, EC 1.14.19.3) is an enzyme that converts between types of fatty acids, which are essential nutrients in the human body. The enzyme mainly catalyzes the chemical reaction
- linoleoyl-CoA + AH2 + O2 gamma-linolenoyl-CoA + A + 2 H2O
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The three substrates of this enzyme are linoleoyl-CoA, an electron acceptor AH2, and O2, whereas its three products are gamma-linolenoyl-CoA, the reduction product A, and H2O.
This enzyme belongs to the family of oxidoreductases, specifically those acting on paired donors, with O2 as oxidant and incorporation or reduction of oxygen. The oxygen incorporated need not be derived from O2 with oxidation of a pair of donors resulting in the reduction of O to two molecules of water. The systematic name of this enzyme class is linoleoyl-CoA,hydrogen-donor:oxygen oxidoreductase. Other names in common use include acyl-CoA 6-desaturase, Delta6-desaturase (D6D or Δ-6-desaturase), Delta6-fatty acyl-CoA desaturase, Delta6-acyl CoA desaturase, fatty acid Delta6-desaturase, fatty acid 6-desaturase, linoleate desaturase, linoleic desaturase, linoleic acid desaturase, linoleoyl CoA desaturase, linoleoyl-coenzyme A desaturase, and long-chain fatty acid Delta6-desaturase. This enzyme participates in linoleic acid metabolism. It employs one cofactor, iron.
The enzyme is molecularly identical across all living things. It is present in animals, plants, fungi, and cyanobacteria.[5][6]
D6D is one of the three fatty acid desaturases present in humans along with Δ-5 and Δ-9, named so because it was thought to desaturate bond between carbons 6 and 7, counting from carboxyl group (with the carboxyl group carbon numbered one). The number 6 in the name of the enzyme has nothing to do with omega-6 fatty acids. In humans, D6D is encoded by the FADS2 gene.
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D6D is upregulated by estrogen,[9] low levels of omega-3s, and moderate food restriction (up to 300%) [citation needed].
D6D activity slows with age, suggested by reductions in GLA and subsequent metabolites.[10][11] Other inhibiting factors include alcohol, radiation, and diabetes [citation needed].
The conversion rate of ALA into DHA is vulnerable to suppression by dietary fatty acids. ALA intake greater than 1% and total polyunsaturated intake above 3% were found to drastically limit synthesis of EPA and DHA.[12]
Felines lack D6D activity in their guts and accumulate systemic linoleic acid.[15] This increase in linoleic acid in cats has an influence in causing the sexual cycle of T. gondii to be restricted to felines, with linoleic acid stimulating T. gondii sexual reproduction.[16]
Wang, C.; Hucik, B.; Sarr, O.; Brown, L. H.; Wells, K. R. D.; Brunt, K. R.; Nakamura, M. T.; Harasim-Symbor, E.; Chabowski, A.; Mutch, D. M. (2023). "Delta-6 desaturase (Fads2) deficiency alters triacylglycerol/fatty acid cycling in murine white adipose tissue". Journal of Lipid Research. 64 (6): 100376. doi:10.1016/j.jlr.2023.100376. PMC 10323924. PMID 37085033. Biagi, P. L.; Bordoni, A.; Hrelia, S.; Celadon, M.; Horrobin, D. F. (1991). "Gamma-linolenic acid dietary supplementation can reverse the aging influence on rat liver microsome delta 6-desaturase activity". Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism. 1083 (2): 187–192. doi:10.1016/0005-2760(91)90041-F. ISSN 0005-2760. PMID 1674661. Gibson, R. A.; Neumann, M. A.; Lien, E. L.; Boyd, K. A.; Tu, W. C. (2012). "Docosahexaenoic acid synthesis from alpha-linolenic acid is inhibited by diets high in polyunsaturated fatty acids". Prostaglandins, Leukotrienes, and Essential Fatty Acids. 88 (1): 139–146. doi:10.1016/j.plefa.2012.04.003. ISSN 0952-3278. PMID 22515943.
- Okayasu T, Nagao M, Ishibashi T, Imai Y (1981). "Purification and partial characterization of linoleoyl-CoA desaturase from rat liver microsomes". Arch. Biochem. Biophys. 206 (1): 21–28. doi:10.1016/0003-9861(81)90061-8. PMID 7212717.