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Proc Natl Acad Sci U S A. 2016 Feb 23;113(8):2212-7. doi: 10.1073/pnas.1525795113. Epub 2016 Feb 8.

Anti-myostatin antibody increases muscle mass and strength and improves insulin sensitivity in old mice.

Author information

1
Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520;
2
Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520; Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06520;
3
Division of Endocrinology and Metabolism, Department of Medicine, University of Pittsburgh, Pittsburgh, PA 15261;
4
Atara Biotherapeutics, Westlake Village, CA 91363;
5
Department of Internal Medicine, Yale University School of Medicine, New Haven, CT 06520; Department of Cellular and Molecular Physiology, Yale University School of Medicine, New Haven, CT 06520; Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520 gerald.shulman@yale.edu.

Abstract

Sarcopenia, or skeletal muscle atrophy, is a debilitating comorbidity of many physiological and pathophysiological processes, including normal aging. There are no approved therapies for sarcopenia, but the antihypertrophic myokine myostatin is a potential therapeutic target. Here, we show that treatment of young and old mice with an anti-myostatin antibody (ATA 842) for 4 wk increased muscle mass and muscle strength in both groups. Furthermore, ATA 842 treatment also increased insulin-stimulated whole body glucose metabolism in old mice, which could be attributed to increased insulin-stimulated skeletal muscle glucose uptake as measured by a hyperinsulinemic-euglycemic clamp. Taken together, these studies provide support for pharmacological inhibition of myostatin as a potential therapeutic approach for age-related sarcopenia and metabolic disease.

KEYWORDS:

aging; insulin resistance; muscle mass; myostatin; sarcopenia

PMID:
26858428
PMCID:
PMC4776508
DOI:
10.1073/pnas.1525795113
[Indexed for MEDLINE]
Free PMC Article

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