The effects of chronic fish oil feeding in rats on protein catabolism induced by recombinant mediators.

The influence of dietary lipid manipulation with menhaden or safflower oil on changes in protein metabolism in rats receiving recombinant interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha/cachectin (TNF), or both combined (COINF) was examined. Whole-body protein kinetics, energy expenditure, nitrogen excretion, and liver and muscle protein synthesis were studied using tracer quantities of L-[1-14C]-leucine. Rats fed menhaden oil, high in omega-3 fatty acids, had significantly lower rates of leucine oxidation compared to safflower-fed rats after monokine infusion (P less than .05). However, muscle protein synthetic rates and the specific activity of free leucine in plasma and muscle indicated greater net muscle-protein breakdown in animals fed fish oil or receiving monokines. Rats fed omega-3 fatty acids had significantly larger livers as percent of body weight and more total liver protein than safflower oil controls (P less than .0001). Liver weight was further increased by monokines, particularly TNF and COINF (P less than .001) in both diet groups, suggesting that net hepatic anabolism occurred at the expense of net skeletal protein catabolism. Monokines as a group and COINF significantly decreased whole-body leucine flux and incorporation into protein; no effect of menhaden oil was noted. In addition, monokines increased nitrogen excretion during the 24-hour experimental period (P less than .05), and total energy expenditure rose significantly in all groups receiving IL-1 beta and COINF. The recombinant monokines IL-1 beta and TNF, particularly when coinfused, are able to reproduce many of the protein anabolic and catabolic consequences seen following infection and injury.(ABSTRACT TRUNCATED AT 250 WORDS)