help button home button Endocrine Society Endocrinology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow Request Copyright Permission
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Kveiborg, M.
Right arrow Articles by Baron, R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Kveiborg, M.
Right arrow Articles by Baron, R.
Endocrinology Vol. 143, No. 11 4304-4309
Copyright © 2002 by The Endocrine Society

ARTICLE

The Increased Bone Mass in {Delta}FosB Transgenic Mice Is Independent of Circulating Leptin Levels

M. Kveiborg, R. Chiusaroli, N. A. Sims, M. Wu, G. Sabatakos, W. C. Horne and R. Baron

Departments of Cell Biology and Orthopedics, Yale University School of Medicine, New Haven, Connecticut 06510

Address all correspondence and requests for reprints to: Dr. Roland Baron, Department of Orthopedics and Cell Biology, Yale University, School of Medicine, 333 Cedar Street, SHM IE-55, New Haven, Connecticut 06510. E-mail: roland.baron{at}yale.edu.

Transgenic mice overexpressing {Delta}FosB, a naturally occurring splice variant of FosB, develop an osteosclerotic phenotype. The increased bone formation has been shown to be due, at least in part, to autonomous effects of {Delta}FosB isoforms on cells of the osteoblast lineage. However, abdominal fat and marrow adipocytes are also markedly decreased in {Delta}FosB mice, leading to low serum leptin levels. Increased bone mass has been linked to the absence of leptin and leptin receptor signaling in ob/ob and db/db mice. Thus, in addition to affecting directly osteoblastogenesis and bone formation, {Delta}FosB isoforms might increase bone mass indirectly via a decrease in leptin. To test this hypothesis, we restored normal circulating levels of leptin in {Delta}FosB mice via sc implanted osmotic pumps. Complete histomorphometric analysis demonstrated that trabecular bone volume as well as dynamic parameters of bone formation was unchanged by this treatment in both {Delta}FosB transgenic mice and control littermates. This demonstration that restoring circulating levels of leptin in {Delta}FosB transgenic mice failed to rescue the bone phenotype further indicates that the marked increase in bone formation is autonomous to the osteoblast lineage.




This article has been cited by other articles:


Home page
 EndocrinologyHome page
G. C. Rowe, C. S. Choi, L. Neff, W. C. Horne, G. I. Shulman, and R. Baron
Increased Energy Expenditure and Insulin Sensitivity in the High Bone Mass {Delta}FosB Transgenic Mice
Endocrinology, January 1, 2009; 150(1): 135 - 143.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
D. Inoue, S. Kido, and T. Matsumoto
Transcriptional Induction of FosB/{Delta}FosB Gene by Mechanical Stress in Osteoblasts
J. Biol. Chem., November 26, 2004; 279(48): 49795 - 49803.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Cell. Biol.Home page
M. Kveiborg, G. Sabatakos, R. Chiusaroli, M. Wu, W. M. Philbrick, W. C. Horne, and R. Baron
{Delta}FosB Induces Osteosclerosis and Decreases Adipogenesis by Two Independent Cell-Autonomous Mechanisms
Mol. Cell. Biol., April 1, 2004; 24(7): 2820 - 2830.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
S. Khosla
Editorial: Leptin--Central or Peripheral to the Regulation of Bone Metabolism?
Endocrinology, November 1, 2002; 143(11): 4161 - 4164.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Endocrinology Endocrine Reviews J. Clin. End. & Metab.
Molecular Endocrinology Recent Prog. Horm. Res. All Endocrine Journals
Copyright © 2002 by The Endocrine Society