Good bones; good fertility


A large percentage of men and women who confront infertility never find out why they can’t conceive. Many men never learn the source of their low testosterone. But exciting new research from Columbia University Medical Center shows that the skeleton acts as a regulator of fertility in male mice and does so through a hormone called osteocalcin.

Gerard Karsenty, MD, PhD, chair of the Department of Genetics and Development at Columbia, led the team whose research will be published online in Cell.

Interaction between skeletal system and reproductive system is not new. There has long been interest in the influence of the gonads 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 questions: Does bone regulate the gonads?” said Dr. Karsenty.

They looked at the reproductive activity of mice. Researchers observed that males whose skeletons did not secrete osteocalcin had smaller litters. The researchers then did experiments to see how osteocalcin promotes the production of testosterone. When they added osteocalcin to cells that produce testosterone, its synthesis increased. Similarly, when they injected osteocalcin directly into male mice, testosterone also went up.

When osteocalcin is not present, testosterone levels drop. Sperm counts goes down and so do the number of offspring.

Though this hasn’t been confirmed in humans, physiology is similar enough between mice and men to make some assumptions. 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.

Source: Columbia University Medical Center, ScienceDaily


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