ONTOGENY OF GROWTH-HORMONE, INSULIN-LIKE GROWTH-FACTOR-I, ESTRADIOL AND CORTISOL IN THE GROWING LAMB - EFFECT OF TESTOSTERONE

Citation
Am. Arnold et al., ONTOGENY OF GROWTH-HORMONE, INSULIN-LIKE GROWTH-FACTOR-I, ESTRADIOL AND CORTISOL IN THE GROWING LAMB - EFFECT OF TESTOSTERONE, Journal of Endocrinology, 150(3), 1996, pp. 391-399
Citations number
35
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
00220795
Volume
150
Issue
3
Year of publication
1996
Pages
391 - 399
Database
ISI
SICI code
0022-0795(1996)150:3<391:OOGIGE>2.0.ZU;2-S
Abstract
Exogenous sex steroids have altered growth hormone secretion in some d omestic species. This study examined whether different physiological c oncentrations of testosterone alter muscle growth in sheep through mod ification of the somatotropic axis. The effects of testosterone on gro wth hormone (GH), insulin-like growth factor-I (IGF-I), estradiol (E(2 )) and cortisol concentrations in growing lambs were evaluated in 20 r ams, 20 wethers and 20 wethers receiving subcutaneous testosterone rep lacement therapy. Two animals from each of the three testosterone stat us groups were slaughtered at 14-day intervals from 49 to 133 days of age, and then at 28-day intervals until 217 days of age for a total of 10 slaughter ages. Animals were sampled every 10 min for an 8-h perio d 1 day prior to slaughter to characterize the episodic patterns of GH and testosterone. Immediately after slaughter, the semi-tendinosus, s plenius and triceps brachii muscles were removed, trimmed of adhering fat and connective tissue, and weighed. Testosterone increased the com bined muscle weight. GH concentrations decreased during the course of the experiment. However, there was no effect of testosterone on GH mea n, baseline, amplitude or GH pulse frequency measured by PULSAR. IGF-I concentrations increased in response to testosterone treatment. Testo sterone had no effect on cortisol levels while E(2) levels were increa sed after 133 days. Increased muscle growth due to testosterone appear ed to be caused either by a direct effect or by increased levels of IG F-I independent of circulating GH concentrations.