β-Hydroxy-β-methylbutyrate (HMB) prevents dexamethasone-induced myotube atrophy

被引：48

作者：

Aversa, Zaira ^{[1
,2
]}

Alamdari, Nima ^{[1
]}

Castillero, Estibaliz ^{[1
]}

Muscaritoli, Maurizio ^{[2
]}

Rossi Fanelli, Filippo ^{[2
]}

Hasselgren, Per-Olof ^{[1
]}

机构：

[1] Harvard Univ, Sch Med, Beth Israel Deaconess Med Ctr, Dept Surg, Boston, MA 02115 USA

[2] Univ Rome, Dept Clin Med, Rome, Italy

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2012年 / 423卷 / 04期

关键词：

Muscle wasting; Glucocorticoids; Atrogin-1; MuRF1; Protein synthesis; Protein degradation; TUMOR-NECROSIS-FACTOR; SKELETAL-MUSCLE; PROTEIN-DEGRADATION; STEROID MYOPATHY; ANGIOTENSIN-II; CULTURED L6; ATTENUATION; PROTEOLYSIS; MECHANISM; CANCER;

D O I：

10.1016/j.bbrc.2012.06.029

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

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.

引用

页码：739 / 743

页数：5

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