Methionine (Met) is a source of sulphur required for the synthesis of cysteine and taurine (Tau) as well as an essential methyl-donor in cellular metabolism. A total of 48% of dietary Met metabolism takes place in the liver. The maintenance of methyl groups and homocysteine homeostasis in the hepatic tissue is dependent on the balance between S-adenosylhomocysteine (SAH) and its precursor, a powerful inhibitor of transmethylation reactions, S-adenosylmethionine (SAM). This SAM:SAH ratio can be affected by S-adenosylhomocysteine hydrolase (SAHH) activity which is involved in the hydrolysis of SAH to homocysteine and adenosine. Homocysteine is a sulphur amino acid metabolite derived from Met. Homeostasis of homocysteine is dependent on genetic factors and nutrient intake (i.e. folate, vitamins B6, B12) and it can be regulated via conversion of homocysteine back to Met (reethylation) or transition to cysteine and Tau (trans-sulfuration) in reactions requiring cystathionine β-synthase (CBS). Amino acids such as serine and glycine have been shown to alleviate methionine toxicity by enhancing formation of cystathionine/cysteine and increasing the activity of cystathionine β-synthase (CBS) ultimately removing an excess of homocysteine. The remethylation of homocysteine in the liver in the process of Met regeneration can also be affected by dietary sulphur amino acid levels, such as cystine, through increase or decrease of betaine-homocysteine methyltransferase (BHMT). Therefore, the objective of the present experiment was to investigate the effect of dietary methionine concentration and alternating feeding strategies in methionine delivery, on the mRNA transcript levels of genes involved in methionine metabolism: SAHH, BHMT, and CBS in Atlantic salmon (Salmo salar) juveniles.

Dietary methionine in salmonid fish feed alters the expression of genes involved in methionine metabolism

TEROVA, GENCIANA;SAROGLIA, MARCO;
2014-01-01

Abstract

Methionine (Met) is a source of sulphur required for the synthesis of cysteine and taurine (Tau) as well as an essential methyl-donor in cellular metabolism. A total of 48% of dietary Met metabolism takes place in the liver. The maintenance of methyl groups and homocysteine homeostasis in the hepatic tissue is dependent on the balance between S-adenosylhomocysteine (SAH) and its precursor, a powerful inhibitor of transmethylation reactions, S-adenosylmethionine (SAM). This SAM:SAH ratio can be affected by S-adenosylhomocysteine hydrolase (SAHH) activity which is involved in the hydrolysis of SAH to homocysteine and adenosine. Homocysteine is a sulphur amino acid metabolite derived from Met. Homeostasis of homocysteine is dependent on genetic factors and nutrient intake (i.e. folate, vitamins B6, B12) and it can be regulated via conversion of homocysteine back to Met (reethylation) or transition to cysteine and Tau (trans-sulfuration) in reactions requiring cystathionine β-synthase (CBS). Amino acids such as serine and glycine have been shown to alleviate methionine toxicity by enhancing formation of cystathionine/cysteine and increasing the activity of cystathionine β-synthase (CBS) ultimately removing an excess of homocysteine. The remethylation of homocysteine in the liver in the process of Met regeneration can also be affected by dietary sulphur amino acid levels, such as cystine, through increase or decrease of betaine-homocysteine methyltransferase (BHMT). Therefore, the objective of the present experiment was to investigate the effect of dietary methionine concentration and alternating feeding strategies in methionine delivery, on the mRNA transcript levels of genes involved in methionine metabolism: SAHH, BHMT, and CBS in Atlantic salmon (Salmo salar) juveniles.
2014
Terova, Genciana; Kwasek, K; Lee, Bg; Saroglia, Marco; Dabrowski, K.
File in questo prodotto:
Non ci sono file associati a questo prodotto.

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11383/1960120
Citazioni
  • ???jsp.display-item.citation.pmc??? ND
  • Scopus ND
  • ???jsp.display-item.citation.isi??? ND
social impact