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-[1-14C]leucine in vivo, 14CO2 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-[1-14C]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.
Costelli
P
P
Dipartimento di Medicina ed Oncologia Sperimentale, Università di Torino, Italy.
Llovera
M
M
García-Martínez
C
C
Carbó
N
N
López-Soriano
F J
FJ
Argilés
J M
JM
D000818:Animals; D002100:Cachexia / Q000209:etiology; D002245:Carbon Dioxide / Q000378:metabolism*; D002976:Clenbuterol / Q000494:pharmacology*; D007930:Leucine / Q000378:metabolism*; D008114:Liver Neoplasms, Experimental / Q000378:metabolism*; D008297:Male; D009132:Muscles / Q000473:pathology; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar
D002245:Carbon Dioxide; D007930:Leucine; D002976:Clenbuterol