February 22, 2011
Male Fertility Is In The Bones
(Ivanhoe Newswire) "“ Scientists have discovered an unexpected connection between a hormone produced in bone and male fertility. The study illustrates that the skeletal hormone known as osteocalcin boosts testosterone production to support the survival of the germ cells that go on to become mature sperm.
According to Gerard Karsenty of Columbia University, the findings in mice offer the foremost evidence that the skeleton controls reproduction through the production of hormones.
Bone was once thought of as a "mere assembly of inert calcified tubes," the researchers explained. Conversely, in the last ten years, scientists have gained a much more dynamic picture of bone as a bona fide endocrine organ with links to energy metabolism and reproduction.
Previous work on skeletal ties to reproduction had focused first and foremost on the reproductive organs as a regulator of bone remodeling. Ultimately, that notion led Karsenty's and his team to once again bone up on their study and particularly focus on whether the influence might go the other way as well. Given the links between menopause and osteoporosis, his team anticipated such a connection would more likely turn up in females, however, that's not what they found at all.
"We found that the bones do control reproduction, but only in males," Karsenty was quoted as saying. "That was obviously a surprise, but that's the finding."
Researchers report that osteocalcin produced by the bone-building cells known as osteoblasts induces testosterone production by the testes, but in due course fails to influence estrogen production by ovaries.
Mating between normal females and osteocalcin-deficient males produced smaller and less frequent litters than those between typical males and females. Males lacking a second gene that inhibits osteocalcin's endocrine functions showed just the opposite: larger (though not significantly larger) and more frequent litters.
The researchers further demonstrated that osteocalcin works through a receptor found on testosterone-producing Leydig cells in the testes. The recently identified osteocalcin receptor is formerly known to be solely expressed in human testicles but not ovaries. Osteocalcin has also been revealed to influence glucose metabolism in both mice and humans, suggesting that it does act as a hormone in humans.
The novel breakthrough could lead to answers for some men who now suffer from unexplained infertility. "Male subfertility with no apparent cause is a well-known condition," Karsenty said. He added that researchers might now start looking for evidence that mutations in osteocalcin or its receptor may be responsible in some of those cases.
Karsenty concludes that his team intends to carry on their study with the effects of bone on male fertility in greater detail, and may discover additional links to female fertility that are independent of osteocalcin.
SOURCE: Cell, February 2011