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leptin regulates bone formation via the sympathetic nervous systemWe previously showed that leptin inhibits bone formation by an undefined mechanism. Here, we show that hypothalamic leptin-dependent antiosteogenic and anorexigenic networks differ, and that the peripheral mediators of leptin antiosteogenic function appear to be neuronal. Neuropeptides mediating leptin anorexigenic function do not affect bone formation. Leptin deficiency results in low sympathetic tone, and genetic or pharmacological ablation of adrenergic signaling leads to a leptin-resistant high bone mass. beta-adrenergic receptors on osteoblasts regulate their proliferation, and a beta-adrenergic agonist decreases bone mass in leptin-deficient and wild-type mice while a beta-adrenergic antagonist increases bone mass in wild-type and ovariectomized mice. None of these manipulations affects body weight. This study demonstrates a leptin-dependent neuronal regulation of bone formation with potential therapeutic implications for osteoporosis.
Document ID
20040088007
Document Type
Reprint (Version printed in journal)
Authors
Takeda, Shu
(Department of Molecular and Human Genetics One Baylor Plaza, Houston, TX 77030, United States)
Elefteriou, Florent
Levasseur, Regis
Liu, Xiuyun
Zhao, Liping
Parker, Keith L.
Armstrong, Dawna
Ducy, Patricia
Karsenty, Gerard
Date Acquired
August 21, 2013
Publication Date
November 1, 2002
Publication Information
Publication: Cell
Volume: 111
Issue: 3
ISSN: 0092-8674
Subject Category
Life Sciences (General)
Funding Number(s)
CONTRACT_GRANT: DK54480
CONTRACT_GRANT: DK58883
CONTRACT_GRANT: HD24054
Distribution Limits
Public
Copyright
Other
Keywords
NASA Discipline Regulatory Physiology
Non-NASA Center