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

被引:27
作者
COSTELLI, P
LLOVERA, M
GARCIAMARTINEZ, C
CARBO, N
LOPEZSORIANO, FJ
ARGILES, JM
机构
[1] UNIV BARCELONA,FAC BIOL,DEPT BIOQUIM & FISIOL,UNITAT BIOQUIM & BIOL MOLEC B,E-08071 BARCELONA,SPAIN
[2] UNIV TURIN,DIPARTIMENTO MED & ONCOL SPERIMENTALE,SEZ PATOL GEN,TURIN,ITALY
关键词
CLENBUTEROL; LEUCINA; TUMOR; CACHEXIA;
D O I
10.1016/0304-3835(94)03719-Y
中图分类号
R73 [肿瘤学];
学科分类号
100214 ;
摘要
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.
引用
收藏
页码:73 / 78
页数:6
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