Journal
MOLECULAR METABOLISM
Volume 5, Issue 10, Pages 1042-1047Publisher
ELSEVIER SCIENCE BV
DOI: 10.1016/j.molmet.2016.07.002
Keywords
Osteocalcin; Muscle mass; Aging
Categories
Funding
- NIAID NIH HHS [T32 AI106711] Funding Source: Medline
- NIAMS NIH HHS [R01 AR045548] Funding Source: Medline
- NIA NIH HHS [P01 AG032959] Funding Source: Medline
- NIDDK NIH HHS [R01 DK104727] Funding Source: Medline
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Objective: A decrease in muscle protein turnover and therefore in muscle mass is a hallmark of aging. Because the circulating levels of the bone-derived hormone osteocalcin decline steeply during aging in mice, monkeys and humans we asked here whether this hormone might regulate muscle mass as mice age. Methods: We examined muscle mass and strength in mice lacking osteocalcin (Ocn-/-) or its receptor in all cells (Gprc6a-/-) or specifically in myofibers (Gprc6a(Mck)-/-) as well as in 9 month-old WT mice receiving exogenous osteocalcin for 28 days. We also examined protein synthesis in WT and Gprc6a-/- mouse myotubes treated with osteocalcin. Results: We show that osteocalcin signaling in myofibers is necessary to maintain muscle mass in older mice in part because it promotes protein synthesis in myotubes without affecting protein breakdown. We further show that treatment with exogenous osteocalcin for 28 days is sufficient to increase muscle mass of 9-month-old WT mice. Conclusion: This study uncovers that osteocalcin is necessary and sufficient to prevent age-related muscle loss in mice. (C) 2016 The Author(s). Published by Elsevier GmbH.
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