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Endocrine Abstracts (2017) 49 S7.2 | DOI: 10.1530/endoabs.49.S7.2

ECE2017 Symposia Crosstalk between bone & other organ(ism)s (3 abstracts)

Osteocalcin signaling in myofibers is necessary and sufficient to increase exercise capacity

Gerard Karsenty


USA.


The observation that circulating osteocalcin levels double during exercise in young mice suggests that this hormone might be a long sought after endocrine regulator of exercise capacity. We addressed this question by analyzing mice lacking either osteocalcin or its receptor in myofibers only. This analysis showed that osteocalcin signaling in myofibers enhances adaptation to exercise because it increases uptake and utilization of glucose into the tricarboxylic acid cycle and promotes fatty Osteocalcin signaling in myofibers favors adaptation to exercise through a second mechanism. Indeed it up-regulates the expression of Interleukin-6 a myokine that favors adaptation to exercise in part by signaling in bone to promote the production of bioactive osteocalcin. Acids utilization. In the course of these studies we noticed that circulating osteocalcin levels decline sharply before mid-life and do not increase during exercise in older mice. This observation raised the prospect that osteocalcin may also be sufficient to correct the age-related decline in muscle function. In support of this hypothesis, our experiments show that exogenous osteocalcin increases the exercise capacity of young wilt-type mice and confers to 15 month-old mice the exercise capacity of 3 month-old mice. This study uncovers an osteocalcin-interleukin-6 axis that increases muscle function during exercise and can reverse the age-induced decline in exercise capacity.

Volume 49

19th European Congress of Endocrinology

Lisbon, Portugal
20 May 2017 - 23 May 2017

European Society of Endocrinology 

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