Increased bone mass in a calcitonin knockout mouse full of surprises

December 17, 2002

Find below one highlighted articles and the full Table of Contents for the December 16 issue.

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Increased bone mass in a calcitonin knockout mouse full of surprises

Bone is in a constant state of remodeling, during which osteoclasts remove old bone (resorption) and osteoblasts form new bone (formation). Calcitonin is a hormone produced by the thyroid gland and inhibits bone resorption. Following menopause, the rate of bone loss is accelerated, however women with post-menopausal osteoporosis that are treated with calcitonin (by injection or nasal spray) demonstrate increased bone mass and strength, in addition to a decrease in the rate of bone fractures. Following alternative processing, the gene encoding calcitonin (CT/CGRP) also encodes a second peptide: calcitonin gene-related peptide-a (CGRPa), however the role of this peptide in bone metabolism has not been clearly defined.

To better understand the role of calcitonin and CGRP-a in bone metabolism Robert Gagel and colleagues at the University of Texas M.D. Anderson Cancer Center, USA, created mice in which the CT/CGRP gene had been deleted. Given that both calcitonin and CGRP have been shown to inhibit bone resorption and CGRP is known to stimulate bone formation, the authors predicted that there would be either no effect of this deletion on bone mass, or there could be some bone loss.

In the December 16 issue of the Journal of Clinical Investigation, the authors report their surprising finding that CT/CGRP-deficient mice have greater bone mass, increased bone formation, and were able to maintain bone mass during estrogen deficiency by increasing bone formation. These findings suggest an important and novel function for the products of the CT/CGRP gene, that was previously unrecognized. They also suggest that the development of an antagonist to the CT/CGRP gene product(s) may be useful in the prevention of bone loss associated with estrogen deficiency.

Mone Zaidi and colleagues from the Mount Sinai Bone Program at Mount Sinai Hospital, New York, discuss these surprising findings in their accompanying commentary.

CONTACT:
Robert F. Gagel
The University of Texas M.D. Anderson Cancer Center
Department of Endocrine Neoplasia and Hormonal Disorders
1400 Holcombe Blvd.
Box 433
Houston, TX 77030
USA
Phone: 713-792-6517
Fax: 713-794-1818
E-mail: rgagel@mdanderson.org

View this article at: http://www.jci.org/cgi/content/full/110/12/1849

ACCOMPANYING COMMENTARY: Calcitonin and bone formation: a knockout full of surprises

CONTACT:
Mone Zaidi
Mount Sinai School of Medicine
Annenberg 5, PO 1055
Division of Endocrinology
One Gustave Levy Place
New York, NY 10029
USA
Phone: 212-241-8797
Fax: 212-426-8312
E-mail: mone.zaidi@mssm.edu

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**Please mention the Journal of Clinical Investigation as the source of these articles**

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