Osteoporosis Theories Fractured

December 10th, 2008 | Sources: Cell, NY Times

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Scientists from Columbia University are reporting that osteoporosis, a chronic bone-wasting condition that affects 10 million elderly Americans, may be mediated by serotonin, a compound previously known for its role in brain functioning.

The astonishing conclusion appears in the journal Cell.

Scientists had known for years that a rare, inherited brittle bone disease was caused by a mutation of a gene known as LRP5. More recently, a second mutation of LRP5 was reported to cause just the opposite—bones so dense that tooth extractions became nearly impossible.

So something was up with LRP5, and the tempting assumption was that the gene directly impacted bone formation.

Not so, according to Gerard Karsenty and colleagues. They proved that LRP5 blocks production of serotonin in the gut.

Then they proved that while gut serotonin has no impact on brain functioning, it does impair bone formation after travelling there through the blood stream.

“We made mice with the inactivated gene,” Dr. Karsenty told the New York Times. These mice had 4 times the normal levels of circulating gut serotonin, and in their bodies “the bone-forming cells are on strike,” he added.

The mice developed marked osteoporosis.

Karsenty’s team then harvested bone cells from the brittle boned mice and proved in the laboratory that the cells were perfectly capable of normal development and functioning, so long as they were not bathed in serotonin.

Karsenty’s team hopes its work might prompt development of a drug that suppresses gut serotonin synthesis and thus stimulate bone growth in osteoporosis patients.


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