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

Methionine (Met) is a source of sulphur required for the synthesis
of cysteine and taurine as well as an essential methyl-donor
in cellular metabolism. The objective of the present study was to
investigate the effect of dietary Met concentration and alternating
feeding strategies in Met delivery, on the mRNA transcript
levels of genes involved in Met resynthesis (betaine-homocysteine
methyltransferase, BHMT; S-adenosylhomocysteine hydrolase,
SAHH) and net Met loss (taurine synthesis) (cystathionine
beta-synthase, CBS) in Atlantic salmon (Salmo salar) liver.
Salmon alevins (265±3 mg) were distributed into 24 tanks (50
fish per tank; 3 replicates). The experimental diets were supplemented
with L-Met at 0, 1.9, 5.8, and 17.4 g/kg (M0, M1/3, M1,
and M3, respectively). The M3 diet without glycine was prepared
to examine Met toxicity (M3-G). These diets were provided via
‘mono-feeding strategy’ meaning fish were fed a designated single
diet. This experiment also included alternative feeding
groups with ‘duo-feeding’ strategy: AF1 (fish fed M0 for 2 days
followed by M1 for 1 day), AF2 (fish fed M0 for 2 days followed by
M3 for 1 day), and AF3 (fish fed two meals of M0 followed by one
meal of M3). Salmon fed M0 diet had smaller weight compared to
all other groups. There was no effect of alternative feeding on the
growth except for the M0 group. The highest expression of CBS
gene was found in the M0, M1/3, and AF-1 groups compared to
M3 and M3-G groups. The expression of CBS gene in the M1
group was lower compared to the AF-1 group. The expression of
SAHH gene was the highest in the M3 group compared to M1,
M1/3, and AF-3 groups. The highest expression of BHMT gene
was found in the M0, M1/3, and AF-1 groups indicating enhanced re-methylation of homocysteine by betaine to Met. The lowest
BHMT expression in M1, M3, M3-G, AF-2, and AF-3 groups compared
to other treatments can be indicative of downregulation of
remethylation in the liver. In conclusion, the present study found
that dietary Met can directly affect the expression of genes
involved in its hepatic metabolism. Although the alternate provision
of Met in a form of combination of low and high Met containing
diets seems to support its efficient utilization in the
salmon liver, there is no evidence that this strategy will be compensating
enough in the case of inadequate Met levels.