Leptin-dependent co-regulation of bone and energy metabolism.

Vijay K. Yadav, Gerard Karsenty

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27 Citas (Scopus)

Resumen

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.

Idioma originalEnglish
Páginas (desde-hasta)954-956
Número de páginas3
PublicaciónAging
Volumen1
N.º11
DOI
EstadoPublished - nov. 2009

Financiación

FinanciadoresNúmero del financiador
National Institute of Diabetes and Digestive and Kidney DiseasesK99DK085328

    ASJC Scopus Subject Areas

    • Ageing
    • Cell Biology

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    Profundice en los temas de investigación de 'Leptin-dependent co-regulation of bone and energy metabolism.'. En conjunto forman una huella única.

    Citar esto

    Yadav, V. K., & Karsenty, G. (2009). Leptin-dependent co-regulation of bone and energy metabolism. Aging, 1(11), 954-956. https://doi.org/10.18632/aging.100100