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    Endocrine Regulation of Male Fertility by the Skeleton

    Cell. 2011 Feb 16. [Epub ahead of print]

    Using co-culture assays, the authors demonstrate that osteoblast cultures are able to induce testosterone production by the testes. Interestingly, they fail to demonstrate an effect of osteoblasts on estrogen production by the ovaries. Analyses of cell-specific loss- and gain-of-function models revealed that the osteoblast-derived protein osteocalcin was the factor that regulated testicular androgen production.
    Authors: Oury F, Sumara G, Sumara O, et. al

    Interactions between bone and the reproductive system have until now been thought to be limited to the regulation of bone remodeling by the gonads. We now show that, in males, bone acts as a regulator of fertility. Using coculture assays, we demonstrate that osteoblasts are able to induce testosterone production by the testes, though they fail to influence estrogen production by the ovaries. Analyses of cell-specific loss- and gain-of-function models reveal that the osteoblast-derived hormone osteocalcin performs this endocrine function. By binding to a G protein-coupled receptor expressed in the Leydig cells of the testes, osteocalcin regulates in a CREB-dependent manner the expression of enzymes that is required for testosterone synthesis, promoting germ cell survival. This study expands the physiological repertoire of osteocalcin and provides the first evidence that the skeleton is an endocrine regulator of reproduction.

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