Reach further, in an Open Access Journal Endocrinology, Diabetes & Metabolism Case Reports

ISSN 1470-3947 (print)
ISSN 1479-6848 (online)

Searchable abstracts of presentations at key conferences in endocrinology

Published by BioScientifica
Endocrine Abstracts (2012) 29 S36.1 

Leptin and bone signaling

S. Takeda

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Osteoporosis is caused by a failure of bone homeostasis. The precise molecular mechanism controlling bone homeostasis is largely unknown. Increasing evidences that neurons and neurotransmitters are intimately involved in bone remodeling shed light on a novel regulatory mechanism for bone homeostasis. Namely, like all other homeostatic functions, bone remodeling is under the control of hypothalamus. We have uncovered that leptin, an adipocyte-derived anorexigenic hormone, regulates bone mass through its receptor located in the central nervous system. Subsequent analysis revealed that leptin uses sympathetic nervous system to inhibit bone formation and stimulate bone resorption. Furthermore, serotonin has emerged as an indispensable molecule linking leptin, bone and energy metabolism. We also found that NMU, another anorexigenic neuropeptide, is a novel central mediator of leptin-dependent regulation of bone mass. In addition, many epidemiological studies confirmed the effect of beta blockers on bone mass and fracture. We are currently analyzing the bone abnormality in mice lacking other neuropeptides. I will summarize the advance of this brain-bone-adipo axis research field.

Declaration of interest: The authors declare that there is no conflict of interest that could be perceived as prejudicing the impartiality of the research project.

Funding: This work was supported, however funding details are unavailable.

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