This is the authors' abstract. We don't add key points for this paper.
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.
Answers are grounded in this paper and cite their sources.
No takes yet. Share an insight, caveat, or question.
Huang et al. (1998) studied this question.
Synapse has enriched 10 related papers. Consider them for comparative context: