ArticleLipids1999
Metabolism of n-3 and n-6 fatty acids in Atlantic salmon liver: stimulation by essential fatty acid deficiency.
Article in Lipids, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 78 citations in OpenAlex.
- Genetic and metabolic characterization of individual differences in liver fat accumulation in Atlantic salmon.Frontiers in genetics · 2025Article
- Different Dietary Ratios of Camelina Oil to Sandeel Oil Influence the Capacity to Synthesise and Deposit EPA and DHA in Zucker Fa/Fa Rats.Nutrients · 2023Article
- Individual differences in EPA and DHA content of Atlantic salmon are associated with gene expression of key metabolic processes.Scientific reports · 2019Article
- Article
- Low levels of very-long-chainJournal of nutritional science · 2017Article
- Minor lipid metabolic perturbations in the liver of Atlantic salmon (Salmo salar L.) caused by suboptimal dietary content of nutrients from fish oil.Fish physiology and biochemistry · 2016Article
- Regulation of the Omega-3 Fatty Acid Biosynthetic Pathway in Atlantic Salmon Hepatocytes.PloS one · 2016Article
- Atlantic salmon require long-chain n-3 fatty acids for optimal growth throughout the seawater period.Journal of nutritional science · 2016Article
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- Review
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- Characterization of scavenger receptor class B, type I in Atlantic salmon (Salmo salar L.).Lipids · 2006Article
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- Effect of 18:1n-9, 20:5n-3, and 22:6n-3 on lipid accumulation and secretion by Atlantic salmon hepatocytes.Lipids · 2005Article
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- Beta-oxidation of 18:3n-3 in Atlantic salmon (Salmo salar L.) hepatocytes treated with different fatty acids.Lipids · 2004Article
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Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidation, esterification, desaturation, and elongation of [1-14C]18:2n-6 and [1-14C]18:3n-3 were studied using hepatocytes from Atlantic salmon (Salmo salar L.) maintained on diets deficient in n-3 and n-6 polyunsaturated fatty acids (PUFA) or supplemented with n-3 PUFA. For both dietary groups, radioactivity from 18:3n-3 was incorporated into lipid fractions two to three times faster than from 18:2n-6, and essential fatty acids (EFA) deficiency doubled the incorporation. Oxidation to CO2 was very low and was independent of substrate or diet, whereas oxidation to acid-soluble products was stimulated by EFA deficiency. Products from 18:2n-6 were mainly 18:3n-6, 20:3n-6, and 20:4n-6, with minor amounts of 20:2n-6 and 22:5n-6. Products from 18:3n-3 were mainly 18:4n-3, 20:5n-3, and 22:6n-3, with small amounts of 20:3n-3. The percentage of 22:6n-3 in the polar lipid fraction of EFA-deficient hepatocytes was fourfold higher than in n-3 PUFA-supplemented cells. This correlated well with our other results obtained after abdominal injection of [1-14C]18:3n-3 and [1-14C]18:2n-6. In hepatocytes incubated with [4,5-3H]-22:6n-3, 20:5n-3 was the main product. This retroconversion was increased by EFA deficiency, as was peroxisomal betaoxidation activity. This study shows that 18:2n-6 and 18:3n-3 can be elongated and desaturated in Atlantic salmon liver, and that this conversion and the activity of retroconversion of very long chain PUFA is markedly enhanced by EFA deficiency.
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