Testicular function and bone metabolism-beyond testosterone
Ferlin A, Selice R, Carraro U, Foresta C. Nat Rev Endocrinol. 2013 Jul 16. doi: 10.1038/nrendo.2013.135. [Epub ahead of print]

Source

Department of Molecular Medicine, Section of Clinical Pathology & Center for Human Reproduction Pathology, University of Padova, Via Gabelli 63, 35121 Padova, Italy.

Abstract

Findings in the past few years have advanced understanding of the crosstalk between testis and bone and could contribute to defining an improved clinical approach to the biochemical diagnosis and therapeutic management of hypogonadism and male osteoporosis. This Review focuses on the Leydig cells of the testis. Other than being responsible for steroidogenesis and production of testosterone, the function of these cells is fundamental to bone health in at least two other ways: Leydig cells produce insulin-like 3 (INSL3), which has a role in osteoblast function, and they contribute to 25-hydroxylation of vitamin D. Impairment of testicular function leads to low levels of testosterone, INSL3 and 25-hydroxyvitamin D and consequently to an increased risk of osteopenia and osteoporosis.