Washington: The skeleton may be the key to fertility in male mice through a hormone released by it known as osteocalcin, a study suggests, and this could well be the case in humans too.
Until now, interactions between bone and the reproductive system have focused only on the influence of gonads (organs that make gametes, like testes in males) on the build-up of bone mass.
"Since communication between two organs in the body is rarely one-way, the fact that the gonads regulate bone really begs the question - Do bones regulate the gonads?" said Gerard Karsenty, professor of genetics at the Columbia University Medical Centre.
Karsenty and his team found their first clue to an answer in the reproductive success of their lab mice, the journal Cell reports.
Previously, they had observed that males whose skeletons did not secrete a hormone called osteocalcin were poor breeders, according to a Columbia statement.
Several experiments show that osteocalcin enhances the production of testosterone, a sex steroid hormone controlling male fertility.
As they added osteocalcin to cells that, when in our body produce testosterone, its synthesis increased. Similarly, when they injected osteocalcin into male mice, circulating levels of testosterone also went up.
Conversely, when osteocalcin is not present, testosterone levels drop, which causes a decline in sperm count, the researchers found.
Though the findings have not yet been confirmed in humans, Karsenty expects to find similar characteristics in humans, based on other similarities between mouse and human hormones.
If osteocalcin also promotes testosterone production in men, low osteocalcin levels may be the reason why some infertile men have unexplained low levels of testosterone.
"These findings suggest that bone is not just a victim of the aging process, but that it may be an active determinant of aging as well," concludes Karsenty.