Endocrinology of the mammalian fetal testis

Abstract

The testes are essential endocrine regulators of fetal masculinization and male development and are, themselves, subject to hormonal regulation during gestation. This review focuses, primarily, on this latter control of testicular function. Data available suggest that, in most mammalian species, the testis goes through a period of independent function before the fetal hypothalamic-pituitary-gonadal axis develops at around 50% of gestation. This pituitary-independent phase coincides with the most critical period of fetal masculinization. Thereafter, the fetal testes appear to become pituitary hormone-dependent, concurrent with declining Leydig cell function, but increasing Sertoli cell numbers. The two orders of mammals most commonly used for these types of studies (rodents and primates) appear to represent special cases within this general hypothesis. In terms of testicular function, rodents are born 'early' before the pituitary-dependent phase of fetal development, while the primate testis is dependent upon placental gonadotropin released during the pituitary-independent phase of development.

Pathogenesis of germ cell neoplasia in testicular dysgenesis and disorders of sex development

“…The resulting somatic niche is organised to support the germ cells, and -in addition to the Sertoli cells -entails fetal Leydig cells and peritubular myoid cells, the latter evident first from 12 GW [24]. Around the time of their initial appearance (8 GW) the fetal Leydig cells initiate steroidogenesis which is required for fetal masculinisation [32][33][34].…”

Mapping lineage progression of somatic progenitor cells in the mouse fetal testis

“…Despite their similar functions in producing androgens, fetal and adult Leydig cells exhibit many differences in their transcriptomes (Dong et al, 2007;Shima et al, 2013), morphology (Haider, 2004) and regulation (Agelopoulou et al, 1984;Aubert et al, 1985;Baker and O'Shaughnessy, 2001;Dong et al, 2007;El-Gehani et al, 1998;Gangnerau and Picon, 1987;Ma et al, 2004;Majdic et al, 1998;O'Shaughnessy et al, 1998;Patsavoudi et al, 1985;Zhang et al, 2001). These differences between fetal and adult Leydig cells led to the hypothesis that the two Leydig cell populations are in fact distinct cell lineages arising from separate origins (Baker et al, 1999;Haider, 2004;Kerr and Knell, 1988;Lording and De Kretser, 1972;O'Shaughnessy et al, 2003;O'Shaughnessy and Fowler, 2011;Roosen-Runge and Anderson, 1959;Shima et al, 2013). In fact, multiple origins of fetal Leydig cells have been suggested, including Sf1 + nonsteroidogenic interstitial cells originating from the gonadal primordium (Barsoum et al, 2013;Barsoum and Yao, 2010), mesonephros (Merchant-Larios and Moreno-Mendoza, 1998;Val et al, 2006), neural crest (Mayerhofer et al, 1996), coelomic epithelium (Karl and Capel, 1998), and cells residing in the border between gonad and mesonephros (DeFalco et al, 2011).…”

Fetal programming of adult Leydig cell function by androgenic effects on stem/progenitor cells

“…Adult Leydig cells, the main source of blood testosterone in adult males, do not develop until puberty; the only Leydig cells present in the fetal testis are a different fetal generation (19)(20)(21). Consequently, adult Leydig cells must develop from stem/progenitor cells (22,23).…”