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MGI Accession ID: MGI:1352383
J Number: J:60001
Other Accession IDs: Title: Leptin inhibits bone formation through a hypothalamic relay: a central control of bone mass.
Authors: Ducy P; Amling M; Takeda S; Priemel M; Schilling AF; Beil FT; Shen J; Vinson C; Rueger JM; Karsenty G
Journal: Cell
Volume: 100
Issue: 2
Date: 2000 Jan 21
Year: 2000
Pages: 197-207
Review Status: Peer Reviewed

Abstract:

Gonadal failure induces bone loss while obesity prevents it. This raises the possibility that bone mass, body weight, and gonadal function are regulated by common pathways. To test this hypothesis, we studied leptin-deficient and leptin receptor-deficient mice that are obese and hypogonadic. Both mutant mice have an increased bone formation leading to high bone mass despite hypogonadism and hypercortisolism. This phenotype is dominant, independent of the presence of fat, and specific for the absence of leptin signaling. There is no leptin signaling in osteoblasts but intracerebroventricular infusion of leptin causes bone loss in leptin-deficient and wild-type mice. This study identifies leptin as a potent inhibitor of bone formation acting through the central nervous system and therefore describes the central nature of bone mass control and its disorders.

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