L-leucine, beta-hydroxy-beta-methylbutyric acid (HMB) and creatine monohydrate prevent myostatin-induced Akirin-1/Mighty mRNA down-regulation and myotube atrophy

The purpose of this study was to examine if L-leucine (Leu), β-hydroxy-β-methylbutyrate (HMB), or creatine monohydrate (Crea) prevented potential atrophic effects of myostatin (MSTN) on differentiated C2C12 myotubes. After four days of differentiation, myotubes were treated with MSTN (10 ng/ml) for...

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Published in:Journal of the International Society of Sports Nutrition 2014-08, Vol.11 (1), p.38-38
Main Authors: Mobley, Christopher Brooks, Fox, Carlton D, Ferguson, Brian S, Amin, Rajesh H, Dalbo, Vincent J, Baier, Shawn, Rathmacher, John A, Wilson, Jacob M, Roberts, Michael D
Format: Article
Language:English
Subjects:
Athletes
Deoxyribonucleic acid
DNA
Drugs & sports
Gene expression
Genetic aspects
Hogs
Kinesiology
Messenger RNA
Metabolites
Methods
Microscopy
Musculoskeletal system
Physiological aspects
Protein synthesis
Proteins
Studies
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Summary:The purpose of this study was to examine if L-leucine (Leu), β-hydroxy-β-methylbutyrate (HMB), or creatine monohydrate (Crea) prevented potential atrophic effects of myostatin (MSTN) on differentiated C2C12 myotubes. After four days of differentiation, myotubes were treated with MSTN (10 ng/ml) for two additional days and four treatment groups were studied: 1) 3x per day 10 mM Leu, 2) 3x per day 10 mM HMB, 3) 3x per day 10 mM Crea, 4) DM only. Myotubes treated with DM without MSTN were analyzed as the control condition (DM/CTL). Following treatment, cells were analyzed for total protein, DNA content, RNA content, muscle protein synthesis (MPS, SUnSET method), and fiber diameter. Separate batch treatments were analyzed for mRNA expression patterns of myostatin-related genes (Akirin-1/Mighty, Notch-1, Ski, MyoD) as well as atrogenes (MuRF-1, and MAFbx/Atrogin-1). MSTN decreased fiber diameter approximately 30% compared to DM/CTL myotubes (p 
ISSN:1550-2783
1550-2783
DOI:10.1186/1550-2783-11-38