Male fertility is in the bones, shows mice study

WASHINGTON - A new study has discovered that the skeleton acts as a regulator of fertility in male mice through a hormone released by bone-osteocalcin.

Researchers at Columbia University Medical Center, led by Gerard Karsenty, found their first clue to an answer in the reproductive success of their lab mice. Previously, the researchers had observed that males whose skeletons did not secrete a hormone called osteocalcin were poor breeders.

The investigators did several experiments that 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, found the researchers.

When osteocalcin-deficient male mice were bred with normal female mice, the pairs only produced half the number of litters, as did pairs with normal males, along with a decrease in the number of pups per litter.

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.

However, the researchers didn’t find any evidence that the skeleton influences female reproduction.

“We do not know why the skeleton regulates male fertility, and not female. However, if you want to propagate the species, it’s probably easier to do this by facilitating the reproductive ability of males,” added Karsenty.

The findings have been published in online edition of the journal Cell. (ANI)