Early this year, Dr. Karsenty’s team published a study demonstrating that in mice a protein called osteocalcin, which is produced by bone-forming cells called osteoblasts, binds to a specific receptor on cells of the testes. Male mice that were unable to make osteocalcin (as a result of genetic manipulation) produced less testosterone and were less fertile. When they mated, they had fewer and smaller offspring.
Fertility in female mice, on the other hand, was not affected by osteocalcin. Cells in their ovaries lacked the receptors to which the bone hormone binds.
“We were surprised by that,†said Dr. Karsenty. “We thought we’d find a hormone that regulated fertility in both sexes.†Another compound, as yet unknown, may play the analogous role in females, he added.
Human testicular cells also have receptors for the hormone osteocalcin, Dr. Karsenty has found.
“I don’t know of any hormone that functions in mice but not to some extent in humans,†said Thomas Clemens, a researcher at Johns Hopkins University.
Still, the magnitude of the effect may not be the same as in mice.
The main hormone that stimulates testosterone production, in mice and men, is luteinizing hormone, a protein made in the brain. Luteinizing hormone is “the on-off switch†for testosterone, said Dr. Crowley. Osteocalcin, on the other hand, looks more like a “dimmer switch†that modulates the process.
The question: Is it a critical mechanism or a backup system? Does osteocalcin play a widespread role in problems like low sperm count and low testosterone, or is it more peripheral?
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