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Journal of Animal Science, Vol 76, Issue 4 999-1003, Copyright © 1998 by American Society of Animal Science
JOURNAL ARTICLE |
H. Huang, C. Gazzola, G. G. Pegg and M. N. Sillence
Tropical Beef Centre, Central Queensland University, and Department of Primary Industries, Rockhampton, Australia.
Corticosteroid hormones increase the density of beta-adrenoceptors in some tissues and may be able to prevent the anabolic effects of beta-agonists from becoming attenuated. The aim of this study was to find a suitable dose of corticosterone that would up-regulate beta2-adrenoceptors in skeletal muscle without arresting the animal's growth. Male rats were given five daily injections of corticosterone at 0, 6.25, 12.5, 25, or 50 mg/kg. The animals were far more sensitive to the catabolic effects of this steroid than female rats used in a previous study. There was no change in food intake, liver, heart, or soleus muscle mass, but corticosterone caused a dose-related decrease in weight gain, carcass weight, omental fat pad weight, and gastrocnemius/plantaris muscle mass (P < .01). From a regression of muscle mass against dose, we calculated that 4.4 mg x kg(-1) x d(-1) would be the largest dose of corticosterone that a male rat could tolerate without any catabolic effect in skeletal muscle. Corticosterone failed to increase beta-adrenoceptor density at any of the doses tested. We conclude that corticosterone treatment is unlikely to be effective at enhancing the growth response of male rats to beta-agonists.
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