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 tissue protein hypercatabolism and alterations of the hormonal homeostasis in the host. After a single intravenous tracer dose of L-[1-C-14]leucine in vivo, (CO2)-C-14 release by tumour-bearing rats is significantly elevated with respect to the controls, Treatment of the tumour hosts with a beta-adrenergic agonist (clenbuterol) is able to prevent either the depletion of the skeletal muscle mass or the enhanced whole-body leucine oxidation. Incubation of soleus muscles in the presence of L-[1-C-14]leucine indicates an increased ability of the muscle obtained from the tumour hosts to utilize the amino acid for oxidation. Similarly to what is observed in vivo, clenbuterol administration exerts a protective effect reducing the rate of leucine oxidation to the control levels.