ENHANCED LEUCINE OXIDATION IN RATS BEARING AN ASCITES HEPATOMA (YOSHIDA AH-130) AND ITS REVERSAL BY CLENBUTEROL

The growth of the rat ascites hepatoma Yoshida AH-130 causes marked ti ssue protein hypercatabolism and alterations of the hormonal homeostas is in the host. After a single intravenous tracer dose of L-[1-C-14]le ucine in vivo, (CO2)-C-14 release by tumour-bearing rats is significan tly elevated with respect to the controls, Treatment of the tumour hos ts with a beta-adrenergic agonist (clenbuterol) is able to prevent eit her the depletion of the skeletal muscle mass or the enhanced whole-bo dy leucine oxidation. Incubation of soleus muscles in the presence of L-[1-C-14]leucine indicates an increased ability of the muscle obtaine d from the tumour hosts to utilize the amino acid for oxidation. Simil arly to what is observed in vivo, clenbuterol administration exerts a protective effect reducing the rate of leucine oxidation to the contro l levels.