Journal
CELL METABOLISM
Volume 13, Issue 6, Pages 627-638Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2011.03.020
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Funding
- Doris Duke Charitable Foundation
- Department of Veterans Affairs
- American Diabetes Association
- NIAMS/NIH [1R01AR059115-01]
- NIH [T32 GM073610]
- Cardiovascular Interdisciplinary Research Fellowship [HL007121]
- University of Iowa Institute for Clinical and Translational Science
- University of Iowa Research Foundation
- Fraternal Order of Eagles Diabetes Research Center
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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 m RNA 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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