Abstract
Experimental models of acute liver, renal, and hepatorenal damage were induced in rats by intraperitoneal injection of D-galactosamine and bilateral ligation of renal hilus to evaluate changes in the levels of branched-chain amino acids (BCAA), branched-chain ketoacids (BCKA) and alanine in the liver, plasma, and muscle, hepatic energy chage (E. C.: (ATP +O.5ADP)/ATP + ADP + AMP), cytosolic redox state, and mitochondorial redox state after 2 4hours. The results showed that E. C., which reflects intracellular energy state, decreased in each damage group, suggesting deficit in energy supply. After confirmation of this fact, level of BCAA and BCKA, the sources of energy supply were measured, and supply of BCAA by degradation of muscle prtein was observed in muscle tissue. Increased transamination to BCKA was also suggested. Alanine, a glucogenous amino aids was supplied to the liver at the same time. The present results suggest that, under such damages, BCAA supplied from muscle tissue is thought to be transaminazed to BCKA, followed by oxidative decarboxylation in the muscle or liver, and is potentially utilized as an energy source in the muscle and liver. It is suggested that transaminazed and decarboxlized BCKA is utilized as energy in liver damage and renal damage; however, under hepatorenal damage, converted BCKA is not utilized, alanine accumulated, and energy supply by 9 oxidization of fatty acid is suppressed.
