Starvation Induced Alterations in Hepatic Lysine Metabolism in Different Families of Rainbow Trout (Oncorhynchus mykiss)

Abstract

Lysine is the second limiting amino acid in fish meal based diets, second only to methionine. However, little is known about lysine metabolism in rainbow trout (RBT). Therefore, lysine catabolism by the lysine α-ketoglutarate reductase (LKR) pathway was studied. Additionally, since genetically improved strains could influence fish production, these studies were performed in 4 distinct families of RBT. Two full-sibling families, differing in feed efficiency, were selected from each of 2 strains (A and B) of RBT. Eight fish from each of the 4 families were allotted to individual tanks. Fish were fed until satiation for 5 weeks when four fish within each family were randomly selected for 2 weeks of starvation. After the starvation period, all fish were harvested. Hepatic in-vitro LKR activity and lysine oxidation were measured as was LKR mRNA. No effect of family within strain on LKR activity or lysine oxidation was detected. Strain A exhibited a 55% reduction (p < 0.01) in LKR transcripts compared to strain B pooled across both feeding levels. Within each family, LKR mRNA was decreased (p < 0.01) in starved vs. fed fish. On average, there was a 68% decrease in LKR transcripts for starved fish. LKR activity averaged 104 ± 33 and 150 ± 31 nmol/min*gm liver (p > 0.1) in fed and starved fish, respectively. Lysine oxidation averaged 1.2 ± 0.5 and 2.2 ± 0.4 nmol/min*gm liver (p > 0.1) in fed and starved fish, respectively. LKR transcripts were positively correlated to weight gain (p < 0.01). These data are consistent with multiple modes of LKR regulation in fish.