Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 423, Issue 4, Pages 739-743Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2012.06.029
Keywords
Muscle wasting; Glucocorticoids; Atrogin-1; MuRF1; Protein synthesis; Protein degradation
Categories
Funding
- NIH [R01 DK37908]
- Department of Clinical Medicine, Sapienza, University of Rome, Rome, Italy
- Gobierno Vasco, Spain [BFI2010-240]
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High levels of glucocorticoids result in muscle wasting and weakness. beta-hydroxy-beta-methylbutyrate (HMB) attenuates the loss of muscle mass in various catabolic conditions but the influence of HMB on glucocorticoid-induced muscle atrophy is not known. We tested the hypothesis that HMB prevents dexamethasone-induced atrophy in cultured myotubes. Treatment of cultured L6 myotubes with dexamethasone resulted in increased protein degradation and expression of atrogin-1 and MuRF1, decreased protein synthesis and reduced myotube size. All of these effects of dexamethasone were attenuated by HMB. Additional experiments provided evidence that the inhibitory effects of HMB on dexamethasone-induced increase in protein degradation and decrease in protein synthesis were regulated by p38/MAPK- and PI3K/Akt-dependent cell signaling, respectively. The present results suggest that glucocorticoid-induced muscle wasting can be prevented by HMB. (C) 2012 Elsevier Inc. All rights reserved.
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