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Bone Abstracts (2017) 6 IS07 | DOI: 10.1530/boneabs.6.IS07

ICCBH2017 Invited Speaker Abstracts (1) (1) (2 abstracts)

A role for leptin as a myokine mediating muscle-bone interactions

Mark W Hamrick


Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta, Georgia, USA.


Muscle mass and strength are known to enhance pediatric gains in bone mineral and bone cross-sectional area, providing a rationale for targeting muscle early in life as a means of improving bone health. We have recently found that the cytokine-like hormone leptin, a well-established adipokine, is abundant in skeletal muscle. Leptin levels normalized for total protein are actually higher in mouse skeletal muscle than in mouse adipose tissue, and studies in human subjects have demonstrated that muscle actively secretes leptin. The long form of the leptin receptor is abundant in skeletal muscle, and treatment of isolated primary myoblasts with leptin increases the expression of myogenic genes. Leptin treatment in vivo also increases the expression of myogenic microRNAs in skeletal muscle. Finally, recent data suggest that leptin stimulates production of follistatin, a potent antagonist of the atrophy-related factor myostatin. Dietary amino acids such as leucine are thought to induce leptin secretion in adipocytes by activating mTor, and we have shown that the dietary amino acid tryptophan can activate the mTor pathway in skeletal muscle and increase protein levels of muscle-derived leptin and follistatin. These studies point to a key role for leptin in mediating the impact of dietary amino acids on muscle and bone accrual in both children and adults.

Disclosure: The authors declared no competing interests.

Volume 6

8th International Conference on Children's Bone Health

ICCBH 

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