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Differential effects of dexamethasone and clenbuterol on rat growth and on beta(2)-adrenoceptors in lung and skeletal muscle

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Huang, H., Gazzola, C., Pegg, G.G. and Sillence, M.N. (2000) Differential effects of dexamethasone and clenbuterol on rat growth and on beta(2)-adrenoceptors in lung and skeletal muscle. Journal of Animal Science, 78 (3). pp. 604-608. ISSN 0021-8812

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Article Link: https://doi.org/10.2527/2000.783604x


β-adrenergic agonists increase growth rate, but their efficacy is reduced over time as the number of β2-adrenoceptors in muscle decreases. Dexamethasone increases β2-adrenoceptor density in many tissues, but this effect has not been reported in skeletal muscle. In this study, male rats were treated daily for 10 d with either clenbuterol (4 mg/kg of feed), dexamethasone (.2 mg/kg BW, s.c.), or clenbuterol plus dexamethasone. Untreated rats served as controls. Dexamethasone caused a marked suppression of growth rate, which resulted in decreased (P < .001) body weight (−29%), carcass weight (−30%), hind-limb muscles (−22%), omental fat (−22%), and heart weight (−10%). Feed intake was reduced (−26%), but feed conversion efficiency was also impaired (P < .001). Clenbuterol caused a small increase in growth rate (+6%; P < .05), with an increase in leg muscle (+7%; P < .01) and heart mass (+8%; P < .05). Feed efficiency was improved (P < .001) by clenbuterol. Rats given the combined treatment still showed a reduction in growth rate (−81%). Clenbuterol caused only a mild attenuation of the effects of dexamethasone on feed intake, BW, and carcass weight, but reduced the catabolic effect of dexamethasone on hind-limb muscle to only −8%. Clenbuterol caused a slight increase in the affinity β2-adrenoceptors in lung for binding to the radioligand (−)[125I]iodocyanopindolol. Relative to control values, the density of β2-adrenoceptors in lung was +31% with dexamethasone treatment, −45% with clenbuterol, and −23% with the combined treatment. Clenbuterol also decreased β2-adrenoceptors in skeletal muscle (−35%), but so did dexamethasone (−13%), so the effects of the β-adrenergic agonist were not attenuated through use of the combined treatment (−40%). The results show that the inductive effect of glucocorticoids on β2-adrenoceptors is tissue-specific and that glucocorticoid treatment is not a useful adjunct to β-adrenergic agonist treatment in animal production.

Item Type:Article
Subjects:Science > Biology
Animal culture > Laboratory animals
Live Archive:05 Jan 2024 00:37
Last Modified:05 Jan 2024 00:37

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