Effects of clenbuterol on the metabolism of nitrogen and IGF-I level in isolated perfused rat liver.
- Author:
Yuan-Lin ZHENG
1
;
Zheng-Kang HAN
;
Jie CHEN
;
Gen-Tao LIU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Clenbuterol; pharmacology; In Vitro Techniques; Insulin-Like Growth Factor I; metabolism; Liver; drug effects; metabolism; Nitrogen; metabolism; Rats; Rats, Sprague-Dawley
- From: Chinese Journal of Applied Physiology 2002;18(2):169-172
- CountryChina
- Language:Chinese
-
Abstract:
AIMTo examine the liver mechanism with which clenbuterol is explained how to affect growth metabolism.
METHODSTwenty-four adult SD rats were randomly divided into three groups, a control and two treatment groups. The technique of isolated perfused rat liver in vitro was used to study the effects of clenbuterol on urea nitrogen concentration of perfused medium, GPT activity and synthesis and secretion of IGF-I in isolated perfused rat liver.
RESULTSUrea-nitrogen concentration of perfused medium was significantly affected by clenbuterol in a dose-dependent and time-dependent manner. The urea-nitrogen level was decreased by 15.02% (P > 0.05),17.97% (P > 0.05), 26.76% (P < 0.05) and 30.08% (P < 0.01) for 1 h, 2 h, 3 h, 4 h after administering clenbuterol at the dose of 1 x 10(-6) mol/L, respectively, compared to that of control. 1 x 10(-8) mol/L CL had the similar effect on urea-nitrogen level. GTP activity of isolated perfused rat liver was inhibited by clenbuterol. The enzyme activity was decreased by 24.65% (P < 0.05) at the dose of 1 10(-6) mol/L CL in clenbuterol-treated 4h. The production and secretion of IGF-I were also influenced by clenbuterol in isolated perfused rat liver. IGF-I concentration of rat liver was increased by 19.77% (P < 0.05) in 4 h clenbuterol treatment (1 x 10(-6) mol/L). Meanwhile, IGF-I concentration of perfusion medium was also elevated though the difference was not significant compared with control.
CONCLUSIONIt is suggested that clenbuterol may improve growth metabolism by means of increasing nitrogen retention and enhancing IGF-I production and secretion of rat liver.