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Publisert 2016

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Publikasjonsdetaljer

Tidsskrift : Aquaculture Nutrition , vol. 22 , p. 776–785 , 2016

Utgiver : Blackwell Publishing

Internasjonale standardnummer :
Trykt : 1353-5773
Elektronisk : 1365-2095

Publikasjonstype : Vitenskapelig artikkel

Bidragsytere : Espe, Marit; Zerrahn, Jens-Erik; Holen, Elisabeth; Rønnestad, Ivar; Veiseth-Kent, Eva; Aksnes, Anders

Sak : 4

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Kjetil Aune
Bibliotekleder
kjetil.aune@nofima.no

Sammendrag

Phosphatidylcholine is synthesized endogenously through the enzyme phosphatidylethanolamine–methyl transferase. As endogenous choline synthesis requires methyl groups from S-adenosylmethionine (SAM), the endogenous synthesis of choline may depend on SAM availability. SAM availability depends on methionine and ATP. SAM is also a precursor for cysteine and may affect taurine and glutathione concentrations. To investigate whether choline synthesis or transsulphuration is prioritized and the interactions between taurine and choline supplementation when methionine availability is low, juvenile Atlantic salmon were fed low methionine diets with and without taurine and choline supplementation. There were no differences in growth or protein accretion following treatments. Fish fed the low methionine diets did not develop a fatty liver, but choline supplementation increased the concentration of total phospholipids in liver and muscle. Taurine supplementation increased taurine concentrations in liver and muscle, but no interactions with choline were present. Liver SAM was unaffected by treatments. Two of three tanks fed the low methionine diet without choline and taurine supplementation had a higher gene expression of p38MAPK (mitogen activated phosphokinase). Choline supplementation to low methionine diets thus may have beneficial effect on the metabolic health and lipid transport to extra-hepatic tissues. Taurine supplementation had no effect on phospholipids status, but increased taurine concentration in tissues and as such may affect oxidation status when methionine availability is low.

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