PUFA down-regulates the gene expression of elongase and desaturase in ducks
Date Issued
2012
Date
2012
Author(s)
Hui Chong, Hui
Abstract
N-3 polyunsaturated fatty acids (PUFA) can only be obtained directly from the diet or converted from their precursor α-linolenic acid (ALA, 18:3n-3) through a series of chain-elongation and desaturation processes, involving Δ6-desaturase (D6D), Δ5-desaturase (D5D), elongase-2 (Elovl2), elongase-5 (Elovl5) and acyl-CoA oxidase in the liver. While many studies have examined the regulation of these enzymes in mammals, very little is known about their gene expressions in avian species, especially in ducks. Therefore, the purpose of this study was to link fatty acid supplementation to the gene expression of elongase and desaturase in duck liver and primary hepatocytes.
The chicken hepatocellular carcinoma cell line (LMH) and primary liver cells from 7- to 9-day-old unsexed Pekin ducks were treated with PPAR-α agonist WY14643 or PUFAs, including docosahexaenoic acid (DHA) and ALA, and saturated fatty acid palmatic acid (PA). We found that in both systems the hepatic Elovl5, D5D and D6D mRNAs, but not Elovl2, were significantly induced by WY14643, suggesting that PPAR-α induces long-chain PUFA synthesis. By contrast, DHA and ALA treatments significantly reduced the expression of genes tested, except Elovl2, which suggests a negative feedback mechanism existing for the biosynthesis of PUFA. No significant change was found with the PA treatments. We also performed in vivo studies on 7-day-old unsexed ducklings of Pekin and Muscovy, fed with diet supplemented with linseed oil (LO, 1.5% and 3.0%) for 3 weeks. Our results showed that Elovl2, Elovl5 and D5D expressions (as analyzed by RT-qPCR) in liver were slightly, but not significantly, increased by the treatments in Pekin. In addition, Elovl2 was increased by LO in Muscovy. By contrast, Elovl5, D5D and D6D were reduced by 1.5% LO, yet increased by 3.0%, in Muscovy.
In conclusion, we demonstrated here that n-3 PUFA down-regulates the expression of Elovl5, D5D and D6D in duck liver cells, despite not quite consistent for the in vivo experiments. The underlying mechanism remains to be elucidated in the future.
The chicken hepatocellular carcinoma cell line (LMH) and primary liver cells from 7- to 9-day-old unsexed Pekin ducks were treated with PPAR-α agonist WY14643 or PUFAs, including docosahexaenoic acid (DHA) and ALA, and saturated fatty acid palmatic acid (PA). We found that in both systems the hepatic Elovl5, D5D and D6D mRNAs, but not Elovl2, were significantly induced by WY14643, suggesting that PPAR-α induces long-chain PUFA synthesis. By contrast, DHA and ALA treatments significantly reduced the expression of genes tested, except Elovl2, which suggests a negative feedback mechanism existing for the biosynthesis of PUFA. No significant change was found with the PA treatments. We also performed in vivo studies on 7-day-old unsexed ducklings of Pekin and Muscovy, fed with diet supplemented with linseed oil (LO, 1.5% and 3.0%) for 3 weeks. Our results showed that Elovl2, Elovl5 and D5D expressions (as analyzed by RT-qPCR) in liver were slightly, but not significantly, increased by the treatments in Pekin. In addition, Elovl2 was increased by LO in Muscovy. By contrast, Elovl5, D5D and D6D were reduced by 1.5% LO, yet increased by 3.0%, in Muscovy.
In conclusion, we demonstrated here that n-3 PUFA down-regulates the expression of Elovl5, D5D and D6D in duck liver cells, despite not quite consistent for the in vivo experiments. The underlying mechanism remains to be elucidated in the future.
Subjects
Fatty acid
elongase
desaturase
duck
Type
thesis
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