The bone cell-derived hormone osteocalcin promotes the production of testosterone in the mouse testis.
Interestingly, osteocalcin-deficient mice exhibit increased levels of leutenizing hormone (LH), a pituitary hormone that regulates sex steroid synthesis in the testes. Additionally, osteocalcin levels appear to be linked to insulin secretion and sensitivity and circulating levels of testosterone in humans.
In this issue of the Journal of Clinical Investigation, researchers led by Gerard Karsenty at Columbia University conducted a study to determine if LH and insulin regulate osteocalcin's reproductive effects. Using transgenic mice, they found that osteocalcin and LH act in two parallel pathways to stimulate testosterone synthesis.
To determine the importance of osteocalcin in humans, they analyzed patients with primary testicular failure, wherein the testes do not produce enough testosterone, and a mutation in a cellular receptor that allows Leydig cells in the testes to respond to osteocalcin.
This study uncovers an endocrine axis that is necessary for optimal male fertility in the mouse and suggests that osteocalcin modulates reproductive function in humans.
Article: A pancreas-bone-testis axis and conservation of osteocalcin function in humans