Submitted to: Fish Physiology and Biochemistry Journal
Publication Type: Peer reviewed journal
Publication Acceptance Date: 10/31/2005
Publication Date: 3/22/2006
Citation: Higgins, A., Silverstein, J., Engles, J., Wilson, M., Rexroad III, C.E., Blemmings, K. 2006. Starvation induced alterations in hepatic lysine metabolism in different families of rainbow trout (Oncorhynchus mykiss). Fish Physiology and Biochemistry Journal. 31(1):33-44. Interpretive Summary: Aquaculture is rapidly growing in the United States. The USDA estimates that over a billion dollars worth of aquaculture products were sold in 2002 with approximately 40 million pounds of rainbow trout contributing to these sales. As aquaculture expands, research has been aimed at not only reducing production costs but also reducing the environmental impacts. For carnivorous fish, including rainbow trout, acquiring more knowledge about amino acid metabolism will assist in the development of more environmentally sustainable and cost efficient production strategies. Lysine, an essential amino acid, is the second-limiting amino acid next to methionine in fish meal diets, however little is known about lysine metabolism in rainbow trout. Improving lysine utilization in rainbow trout would benefit the aquaculture industry. This study investigated the regulation of lysine alpha-ketoglutarate reductase, a metabolic enzyme which breaks down lysine, during periods of fasting. These studies were performed in 4 genetic groups of rainbow trout tested for feed efficiency to determine if there were relationships between lysine metabolism and fish performance.
Technical 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 alpha-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.