What's Bred in the Bone

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Science  11 Mar 2011:
Vol. 331, Issue 6022, pp. 1243
DOI: 10.1126/science.331.6022.1243-b

In females, the interaction between the reproductive system and bone physiology is well established: Loss of estrogen during aging is a causative factor in osteoporosis. Oury et al. now describe a bone–reproductive system connection in males, where osteocalcin, a hormone produced in bone cells, controls the production of testosterone in the testes. Mice deficient in osteocalcin had smaller testes, decreased concentrations of blood testosterone, and reduced fertility. In the testes, osteocalcin increased expression of genes that participate in testosterone biosynthesis and spermatogenesis and inhibited stem cell death. Osteocalcin probably functions by binding the G protein–coupled receptor Gprc6a, which is specifically expressed in Leydig cells of the testes. Direct binding of osteocalcin to Gprc6a was not directly demonstrated, but mice with reduced expression of Gprc6a in Leydig cells showed impaired testicular function similar to that in osteocalicin-deficient mice. Osteocalcin, which also regulates metabolism through effects on pancreatic beta cells and fat cells, thus appears to have important physiological roles in coordinating energy metabolism, bone remodeling, and reproductive function.

Cell 144, 10.1016/j.cell.2011.02.004 (2011).

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