The role of testosterone in spermatogenesis

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Testosterone production and action is critical for male fertility. An absence of androgen signaling during fetal life results in failure of the urogenital tract to virilize, inhibition of testicular descent, abnormalities in accessory organs, such as the epididymis, prostate and seminal vesicles, and an inability to produce sperm. This chapter focuses on the role of testosterone in the initiation and maintenance of germ cell development, known as spermatogenesis. Much of what we know about testosterone and spermatogenesis is based on studies in which testosterone levels are experimentally manipulated in rodents, non-human primates and men. In recent times, transgenic models have also been utilized extensively and provide important information on the sites and mechanisms of androgen action in spermatogenesis. Luteinizing hormone from the pituitary stimulates the Leydig cells of the testis to produce testosterone, from fetal life through to adulthood. Testosterone is essential for many aspects of spermatogenesis, including meiosis and differentiation of haploid germ cells (a process known as spermiogenesis). Androgen action is primarily mediated by ARs within Sertoli cells; however, AR-mediated action on Leydig cells and peritubular myoid cells is also important. The specific molecular pathways of androgen action are not yet well characterized, with both genomic and non-genomic pathways thought to be involved. While androgen-dependent genes have been discovered, there are surprisingly few. Evidence is emerging that androgens may modulate spermatogenesis by the coordination of transcriptional and translational events, including the regulation of small RNA species that modulate protein expression.

Original languageEnglish
Title of host publicationTestosterone: Action, Deficiency, Substitution, Fourth Edition
PublisherCambridge University Press
Number of pages31
ISBN (Electronic)9781139003353
ISBN (Print)9781107012905
Publication statusPublished - 1 Jan 2012
Externally publishedYes

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