Fatty Acid Desaturase 3 (Fads3) is a singular member of the Fads cluster

Blanchard, H.; Legrand, Philippe; Pédrono, Frédérique

doi:10.1016/j.biochi.2010.03.002

Cited by 29 publications

(28 citation statements)

References 25 publications

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“…The FADS gene cluster has been most extensively studied; it consists of FADS1, FADS2, and FADS3 on chromosome 11 ( 77 ). Although the enzymatic functions of FADS1 and FADS2 are well described, FADS3 remains a gene without a clearly defi ned enzymatic function ( 78 ). More than 20 SNPs have been identifi ed in the FADS gene cluster.…”

Section: Gene Polymorphisms Blood Pufa and Cvdmentioning

confidence: 99%

Omega-3 fatty acid supplementation and cardiovascular disease

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Depner

Tripathy

2012

Journal of Lipid Research

192

118

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Section: Gene Polymorphisms Blood Pufa and Cvdmentioning

confidence: 99%

Omega-3 fatty acid supplementation and cardiovascular disease

Jump

Depner

Tripathy

2012

Journal of Lipid Research

192

118

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“…To preconcentrate the minor FA be a mammalian membrane-bound front-end desaturase. However, no function has been attributed to the FADS3 protein yet ( 15 ).…”

Section: Fatty Acid Analysismentioning

confidence: 99%

Trans-vaccenate is Δ13-desaturated by FADS3 in rodents

Rioux

Pédrono

Blanchard

et al. 2013

Journal of Lipid Research

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This article is available online at http://www.jlr.org "methyl-end" FA desaturases. Therefore, linoleic acid and ␣ -linolenic acid must be provided by the diet ( 3 ). These dietary essential FAs then serve as precursors for longer PUFAs of the n-6 and n-3 series, including arachidonic acid (20:4 n-6) and docosahexaenoic acid (22:6 n-3) required for many important physiological functions in humans ( 4,5 ). In this PUFA biosynthesis, only "front-end" desaturases ( ⌬ 5-and ⌬ 6-desaturases) are involved to introduce new double bonds between the preexisting double bonds and the carboxyl end of FAs ( 6 ).In 2000, the genomic structure of the fatty acid desaturase (FADS) cluster, located on chromosome 11 in humans, was reported ( 7 ). This cluster includes the FADS1 and FADS2 genes that code, respectively, for the well-known ⌬ 5-and ⌬ 6-desaturases involved in PUFA biosynthesis ( 8-10 ). A third gene was identifi ed on this cluster with high degree of nucleotide sequence homology with both FADS1 (62%) and FADS2 (70%) and was therefore named FADS3. Since its fi rst description in humans ( 7 ), FADS3 has been identifi ed in rats ( 11 ), baboons ( 12 ), mice ( 3 ), and many other mammals showing a similar nucleotide sequence and intron/exon organization ( 12 ). When analyzing the peptide sequence deduced from the FADS3 nucleotide sequence, FADS3 protein was identifi ed as a putative desaturase, according to its similarity with FADS1 and FADS2. Indeed, the predicted structure of FADS3 is composed of an N-terminal cytochrome b5-like domain characterized by a HPGG motif shown to be essential for the ⌬ 6-desaturase activity of FADS2 ( 13 ) QIEHH in the rat) characteristic of front-end-desaturases ( 14 ). According to its amino acid sequence, FADS3 was thereafter supposed to Abstract Fatty acid desaturases play critical roles in regulating the biosynthesis of unsaturated fatty acids in all biological kingdoms. As opposed to plants, mammals are so far characterized by the absence of desaturases introducing additional double bonds at the methyl-end site of fatty acids. However, the function of the mammalian fatty acid desaturase 3 (FADS3) gene remains unknown. This gene is located within the FADS cluster and presents a high nucleotide sequence homology with FADS1 ( ⌬ 5-desaturase) and FADS2 ( ⌬ 6-desaturase). Here, we show that rat FADS3 displays no common ⌬ 5-, ⌬ 6-or ⌬ 9-desaturase activity but is able to catalyze the unexpected ⌬ 13-desaturation of trans -vaccenate. Although there is no standard for complete conclusive identifi cation, structural characterization strongly suggests that the ⌬ 11,13-conjugated linoleic acid (CLA) produced by FADS3 from trans -vaccenate is the trans 11, cis 13-CLA isomer. In rat hepatocytes, knockdown of FADS3 expression specifically reduces trans -vaccenate ⌬ 13-desaturation. Evidence is presented that FADS3 is the fi rst "methyl-end" fatty acid desaturase functionally characterized in mammals. FA desaturases introduce double bonds between defi ned carbons of the fatty acyl chain and catalyze ...

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“…Fads5 (or Scd, Scd1) [12][13][14] and Fads4 (or Scd5, Scd4, Scd2) [15][16][17] are stearoyl-CoA delta-9 desaturases with a known role in the synthesis of monounsaturated fatty acids (MUFAs) from saturated fatty acids (SFAs), primarily in the synthesis of oleic acid. Fads6 and Fads3 (or linoleoylCoA delta-9 desaturase-like 3 protein) also play a role in the synthesis of unsaturated fatty acids, but their exact functions have not been defined yet [18]. Fads3 is clustered with Fads1 and Fads2 on human chromosome 11 (11q12-q13.1) [19].…”

Section: Introductionmentioning

confidence: 99%

Fads1 and 2 are promoted to meet instant need for long-chain polyunsaturated fatty acids in goose fatty liver

et al. 2016

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Global prevalence of non-alcoholic fatty liver disease (NAFLD) constitutes a threat to human health. Goose is a unique model of NAFLD for discovering therapeutic targets as its liver can develop severe steatosis without overt injury. Fatty acid desaturase (Fads) is a potential therapeutic target as Fads expression and mutations are associated with liver fat. Here, we hypothesized that Fads was promoted to provide a protection for goose fatty liver. To test this, goose Fads1 and Fads2 were sequenced. Fads1/2/6 expression was determined in goose liver and primary hepatocytes by quantitative PCR. Liver fatty acid composition was also analyzed by gas chromatography. Data indicated that hepatic Fads1/2/6 expression was gradually increased with the time of overfeeding. In contrast, trans-C18:1n9 fatty acid (Fads inhibitor) was reduced. However, enhanced Fads capacity for long-chain polyunsaturated fatty acid (LC-PUFA) synthesis was not sufficient to compensate for the depleted LC-PUFAs in goose fatty liver. Moreover, cell studies showed that Fads1/2/6 expression was regulated by fatty liver-associated factors. Together, these findings suggest Fads1/2 as protective components are promoted to meet instant need for LC-PUFAs in goose fatty liver, and we propose this is required for severe hepatic steatosis without liver injury.

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Fatty Acid Desaturase 3 (Fads3) is a singular member of the Fads cluster

Cited by 29 publications

References 25 publications

Omega-3 fatty acid supplementation and cardiovascular disease

Omega-3 fatty acid supplementation and cardiovascular disease

Trans-vaccenate is Δ13-desaturated by FADS3 in rodents

Fads1 and 2 are promoted to meet instant need for long-chain polyunsaturated fatty acids in goose fatty liver

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