Department of Molecular Medicine, Section of Clinical Pathology & Center for Human Reproduction Pathology, University of Padova, Via Gabelli 63, 35121 Padova, Italy.
Nat Rev Endocrinol. 2013 Sep;9(9):548-54. doi: 10.1038/nrendo.2013.135. Epub 2013 Jul 16.
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.
在过去的几年中，研究结果增进了人们对于睾丸和骨骼之间相互作用的理解，这可能有助于确定改善性腺机能减退症和男性骨质疏松症的生化诊断和治疗管理的临床方法。这篇综述重点介绍了睾丸的间质细胞。除了负责类固醇生成和睾酮的产生外，这些细胞的功能至少还有另外两种方式对骨骼健康至关重要：间质细胞产生胰岛素样因子 3（INSL3），该因子在成骨细胞功能中发挥作用，并且它们有助于维生素 D 的 25-羟化。睾丸功能的损伤会导致睾酮、INSL3 和 25-羟维生素 D 水平降低，从而增加了骨质疏松症和骨量减少的风险。
