Journal article
mRNA Expression Signatures of Human Skeletal Muscle Atrophy Identify a Natural Compound that Increases Muscle Mass
Cell metabolism, Vol.13(6), pp.627-638
2011
DOI: 10.1016/j.cmet.2011.03.020
PMCID: PMC3120768
PMID: 21641545
Abstract
Skeletal muscle atrophy is a common and debilitating condition that lacks a pharmacologic therapy. To develop a potential therapy, we identified 63 mRNAs that were regulated by fasting in both human and mouse muscle, and 29 mRNAs that were regulated by both fasting and spinal cord injury in human muscle. We used these two unbiased mRNA expression signatures of muscle atrophy to query the Connectivity Map, which singled out ursolic acid as a compound whose signature was opposite to those of atrophy-inducing stresses. A natural compound enriched in apples, ursolic acid reduced muscle atrophy and stimulated muscle hypertrophy in mice. It did so by enhancing skeletal muscle insulin/IGF-I signaling and inhibiting atrophy-associated skeletal muscle mRNA expression. Importantly, ursolic acid's effects on muscle were accompanied by reductions in adiposity, fasting blood glucose, and plasma cholesterol and triglycerides. These findings identify a potential therapy for muscle atrophy and perhaps other metabolic diseases.
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► We determined mRNA expression signatures of skeletal muscle atrophy in humans ► Muscle atrophy signatures negatively correlated with the signature of ursolic acid ► Ursolic acid reduced muscle atrophy and induced muscle hypertrophy in mice ► Although ursolic acid increased skeletal muscle mass, it reduced adiposity
Details
- Title: Subtitle
- mRNA Expression Signatures of Human Skeletal Muscle Atrophy Identify a Natural Compound that Increases Muscle Mass
- Creators
- Steven D Kunkel - Department of Internal Medicine, Roy J. and Lucille A. Carver College of Medicine, The University of Iowa, Iowa City, IA 52242, USAManish Suneja - Department of Internal Medicine, Roy J. and Lucille A. Carver College of Medicine, The University of Iowa, Iowa City, IA 52242, USAScott M Ebert - Department of Internal Medicine, Roy J. and Lucille A. Carver College of Medicine, The University of Iowa, Iowa City, IA 52242, USAKale S Bongers - Department of Molecular Physiology and Biophysics, Roy J. and Lucille A. Carver College of Medicine, The University of Iowa, Iowa City, IA 52242, USADaniel K Fox - Department of Molecular Physiology and Biophysics, Roy J. and Lucille A. Carver College of Medicine, The University of Iowa, Iowa City, IA 52242, USASharon E Malmberg - Department of Internal Medicine, Roy J. and Lucille A. Carver College of Medicine, The University of Iowa, Iowa City, IA 52242, USAFariborz Alipour - Department of Speech Pathology and Audiology, Roy J. and Lucille A. Carver College of Medicine, The University of Iowa, Iowa City, IA 52242, USARichard K Shields - Graduate Program in Physical Therapy and Rehabilitation Science, Roy J. and Lucille A. Carver College of Medicine, The University of Iowa, Iowa City, IA 52242, USAChristopher M Adams - Department of Internal Medicine, Roy J. and Lucille A. Carver College of Medicine, The University of Iowa, Iowa City, IA 52242, USA
- Resource Type
- Journal article
- Publication Details
- Cell metabolism, Vol.13(6), pp.627-638
- Publisher
- Elsevier Inc
- DOI
- 10.1016/j.cmet.2011.03.020
- PMID
- 21641545
- PMCID
- PMC3120768
- ISSN
- 1550-4131
- eISSN
- 1932-7420
- Language
- English
- Date published
- 2011
- Academic Unit
- Communication Sciences and Disorders; Molecular Physiology and Biophysics; Orthopedics and Rehabilitation; Physical Therapy and Rehabilitation Science; Nephrology; Internal Medicine
- Record Identifier
- 9984025692602771
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