In a report that appears online today in the journal Nature, Dr. Gerard Karsenty, BCM professor of molecular and human genetics, and his colleagues demonstrate in mice that the sympathetic nervous system mediates the resorption or destruction of bone through a special receptor on bone cells, and that this effect is required for the development of osteoporosis after menopause in mice. Preventing the sympathetic nervous systems from activating this receptor could prevent osteoporosis.

An estimated 10 million Americans over the age of 50 and 30 million people worldwide have osteoporosis, a disease in which there is less bone mass and a high risk of fracture. Each year, 1.5 million Americans suffer a fracture because of the disease. In a report last October, the U.S. Surgeon General estimated that the cost of caring for people with osteoporosis-related fractures totals $18 billion per year, a figure that will increase unless prevention efforts improve.

Karsenty's work started five years ago when his group demonstrated that one of the main functions of leptin, a hormone initially thought only to regulate appetite, is to regulate bone formation. Later, they showed that the sympathetic nervous system mediates only this action of leptin.

In the most recent study, they showed that leptin also affects bone destruction or resorption through a receptor for the sympathetic nervous system present on bone cells.

Mice lacking this receptor have "what every woman at time of menopause would like to experience," said Karsenty. "They make more bone, they destroy less bone and do not lose bone when their ovaries are removed. This is the first demonstration that nerve cells are involved in osteoporosis development. This has
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Contact: Ross Tomlin
htomlin@bcm.tmc.edu
713-798-4712
Baylor College of Medicine
20-Feb-2005