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. 2009 Nov 5;1(11):954-6.
doi: 10.18632/aging.100100.

Leptin-dependent co-regulation of bone and energy metabolism

Affiliations

Leptin-dependent co-regulation of bone and energy metabolism

Vijay K Yadav et al. Aging (Albany NY). .

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.

Keywords: appetite; bone; energy metabolism; leptin; serotonin.

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Conflict of interest statement

The authors of this manuscript have no conflict of interest to declare.

Figures

Figure 1.
Figure 1.. Model of the leptin-dependent central control of bone mass, appetite and energy expenditure.
Leptin inhibits release of brainstem-derived serotonin, which favors bone mass accrual and appetite through its action on hypothalamic neurons. Serotonergic neurons are in blue; VMH, ventromedial hypothalamus; ARC, arcuate; VMH is in purple and arcuate is in green.

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