Research Perspective|Volume 1, Issue 11|pp 954—956

Leptin-dependent co-regulation of bone and energy metabolism

Vijay K. Yadav¹, Gerard Karsenty¹

¹Department of Genetics and Development, Columbia University Medical Centre, New York, NY 10032, USA

Received: October 25, 2009Accepted: November 4, 2009Published: November 5, 2009

Copyright: © 2009 Yadav et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

The adipocyte-derived hormone leptin inhibits appetite and bone mass accrual. To fulfill these two functions leptin requires the integrity of hypothalamic neurons but not the expression of its receptor, ObRb on these neurons. These results suggested that leptin acts first elsewhere in the brain to mediate these functions. However, this neuroanatomical site of leptin action in the brain remained elusive. Recent mouse genetic, electrophysiological and neuroanatomical studies provide evidence that leptin inhibits appetite and bone mass accrual through a two-step pathway: it decreases synthesis and the release by brainstem neurons of serotonin that in turn targets hypothalamic neurons to regulate appetite and bone mass accrual.