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
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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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cited_by cdi_FETCH-LOGICAL-b645t-7c6b89c2685189f8ffa3462c63867366f5d2a58804220c62f10d12239684e7393
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container_title Journal of the International Society of Sports Nutrition
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creator Mobley, Christopher Brooks
Fox, Carlton D
Ferguson, Brian S
Amin, Rajesh H
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Roberts, Michael D
description 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 
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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 &lt; 0.001). Leu, HMB and Crea prevented MSTN-induced atrophy. MSTN did not decrease MPS levels compared to DM/CTL myotubes, but MSTN treatment decreased the mRNA expression of Akirin-1/Mighty by 27% (p &lt; 0.001) and MyoD by 26% (p &lt; 0.01) compared to DM/CTL myotubes. shRNA experiments confirmed that Mighty mRNA knockdown reduced myotube size, linking MSTN treatment to atrophy independent of MPS. Remarkably, MSTN + Leu and MSTN + HMB myotubes had similar Akirin-1/Mighty and MyoD mRNA levels compared to DM/CTL myotubes. Furthermore, MSTN + Crea myotubes exhibited a 36% (p &lt; 0.05) and 86% (p &lt; 0.001) increase in Akirin-1/Mighty mRNA compared to DM/CTL and MSTN-only treated myotubes, respectively. Leu, HMB and Crea may reduce MSTN-induced muscle fiber atrophy by influencing Akirin-1/Mighty mRNA expression patterns. Future studies are needed to examine if Leu, HMB and Crea independently or synergistically affect Akirin-1/Mighty expression, and how Akirin-1/Mighty expression mechanistically relates to skeletal muscle hypertrophy in vivo.</description><identifier>ISSN: 1550-2783</identifier><identifier>EISSN: 1550-2783</identifier><identifier>DOI: 10.1186/1550-2783-11-38</identifier><identifier>PMID: 25132809</identifier><language>eng</language><publisher>United States: BioMed Central Ltd</publisher><subject>Athletes ; Deoxyribonucleic acid ; DNA ; Drugs &amp; sports ; Gene expression ; Genetic aspects ; Hogs ; Kinesiology ; Messenger RNA ; Metabolites ; Methods ; Microscopy ; Musculoskeletal system ; Physiological aspects ; Protein synthesis ; Proteins ; Studies</subject><ispartof>Journal of the International Society of Sports Nutrition, 2014-08, Vol.11 (1), p.38-38</ispartof><rights>COPYRIGHT 2014 BioMed Central Ltd.</rights><rights>2014 Mobley et al.; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.</rights><rights>Copyright © 2014 Mobley et al.; licensee BioMed Central Ltd. 2014 Mobley et al.; licensee BioMed Central Ltd.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-b645t-7c6b89c2685189f8ffa3462c63867366f5d2a58804220c62f10d12239684e7393</citedby><cites>FETCH-LOGICAL-b645t-7c6b89c2685189f8ffa3462c63867366f5d2a58804220c62f10d12239684e7393</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4134516/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/1553676754?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,25731,27901,27902,36989,36990,44566,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25132809$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mobley, Christopher Brooks</creatorcontrib><creatorcontrib>Fox, Carlton D</creatorcontrib><creatorcontrib>Ferguson, Brian S</creatorcontrib><creatorcontrib>Amin, Rajesh H</creatorcontrib><creatorcontrib>Dalbo, Vincent J</creatorcontrib><creatorcontrib>Baier, Shawn</creatorcontrib><creatorcontrib>Rathmacher, John A</creatorcontrib><creatorcontrib>Wilson, Jacob M</creatorcontrib><creatorcontrib>Roberts, Michael D</creatorcontrib><title>L-leucine, beta-hydroxy-beta-methylbutyric acid (HMB) and creatine monohydrate prevent myostatin-induced Akirin-1/Mighty mRNA down-regulation and myotube atrophy</title><title>Journal of the International Society of Sports Nutrition</title><addtitle>J Int Soc Sports Nutr</addtitle><description>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. 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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 &lt; 0.001). Leu, HMB and Crea prevented MSTN-induced atrophy. MSTN did not decrease MPS levels compared to DM/CTL myotubes, but MSTN treatment decreased the mRNA expression of Akirin-1/Mighty by 27% (p &lt; 0.001) and MyoD by 26% (p &lt; 0.01) compared to DM/CTL myotubes. shRNA experiments confirmed that Mighty mRNA knockdown reduced myotube size, linking MSTN treatment to atrophy independent of MPS. Remarkably, MSTN + Leu and MSTN + HMB myotubes had similar Akirin-1/Mighty and MyoD mRNA levels compared to DM/CTL myotubes. Furthermore, MSTN + Crea myotubes exhibited a 36% (p &lt; 0.05) and 86% (p &lt; 0.001) increase in Akirin-1/Mighty mRNA compared to DM/CTL and MSTN-only treated myotubes, respectively. Leu, HMB and Crea may reduce MSTN-induced muscle fiber atrophy by influencing Akirin-1/Mighty mRNA expression patterns. 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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
title L-leucine, beta-hydroxy-beta-methylbutyric acid (HMB) and creatine monohydrate prevent myostatin-induced Akirin-1/Mighty mRNA down-regulation and myotube atrophy
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