Which hormone stimulates the Leydig cells of testes to produce testosterone

The Leydig Cell

Leydig cells have a central role in the synthesis and secretion of testosterone. LH, released from the anterior pituitary, stimulates production of testosterone by the Leydig cell. Many chemicals alter Leydig cell function and some can cause Leydig cell death. For example, ethylene dimethanesulfonate, an agent formerly used for cancer treatment, causes Leydig cell death with subsequent loss of testosterone biosynthesis. A chemical may also disrupt steroidogenesis by its action on the testosterone biosynthetic pathway without causing cell death. For example, δ-9-tetrahydrocannabinol (THC), the active ingredient in cannabis, causes a decline in the release of FSH and LH, resulting in decreased serum levels of testosterone in both experimental animals and humans. Besides disruption to the hypothalamic–pituitary–gonadal axis, THC and its water soluble metabolites can directly reduce cAMP-stimulated testosterone production in Leydig cells.

Leydig Cells

Leydig cells represent a majority of testicular interstitial cells. They produce androgens for normal spermatogenesis and other androgen-target organs beyond the testis (Diemer et al., 2003). Leydig cells also regulate testicular macrophage and lymphocyte numbers (Raburn et al., 1993; Hedger and Meinhardt, 2000). Moreover, rat Leydig cells exhibit antiviral activities by expressing interferons (IFNs) in response to viral infections (Dejucq et al., 1998; Melaine et al., 2003). By contrast, human Leydig cells display relatively weak antiviral activities compared with their rat compartments (Le Tortorec et al., 2008). Mechanisms underlying innate immune responses in mouse Leydig cells have been revealed. Leydig cells constitutively express various pattern recognition receptors (PRRs), including Toll-like receptor 3 (TLR3), TLR4, melanoma differentiation-associated gene 5 (MDA5), retinoic acid-inducible gene I (RIG-I), and p204. TLR4 can be activated by the lipopolysaccharide of Gram-negative bacteria in Leydig cells, thereby initiating innate immune signaling to induce proinflammatory cytokine expression (Shang et al., 2011). TLR3, MDA5, and RIG-I can recognize viral RNA and initiate innate antiviral responses in Leydig cells (Shang et al., 2011; Zhu et al., 2013). DNA sensor p204 also initiates innate antiviral responses in Leydig cells after challenge with viral DNA (Zhu et al., 2014). Thereby, Leydig cells are well equipped with innate defense systems.

Leydig Cells

Leydig cells are another type of interstitial cells, which are responsible for androgen biosynthesis (mostly testosterone and androstenedione), and consequently the regulation of secondary sex characteristics. These include testicular descent, development of prostate, scrotum and penis, and differentiation of the Wolffian duct, which leads to the formation of epididymides, vasa deferentia and seminal vesicles. Fetal Leydig cells are found in the interstitium of the testis shortly after sex determination, and are replaced by adult Leydig cells a few days after birth. Fetal and adult Leydig cells show different gene expression profiles, and it was thought that they derived from different progenitors arising at different time points. Although definitive proof is still lacking, recent studies have suggested the existence of a single progenitor that remains dormant until puberty to then form adult Leydig cells. In addition, the site of origin of fetal Leydig cells is also currently unknown. Some hypotheses suggest that they might arise from the coelomic epithelium, or the mesonephros, or both tissues. Some evidence, instead, supports the view that Leydig cells differentiate from progenitor cells within the testis rather than from a migratory cell population. Indeed, it was shown that Leydig cells appeared in the testis even when this was experimentally dissociated from the mesonephros in vitro. However, data are still not conclusive given the possibility that migration of progenitor cells might have occurred before the time gonad and mesonephros were dissociated. Recently, it was proposed that fetal (and maybe also adult) Leydig cells differentiate from the same Sf1-positive supporting cells that give rise to Sertoli cells. SF1, in fact, is required for the expression of steroidogenic genes including Cyp11a and Star. At the same time, a small fraction of fetal Leydig cells seem to originate from different, Sf1-negative precursors at the mesonephric-gonadal junction.

Desert hedgehog (DHH), which is secreted by Sertoli cells, is necessary for Leydig cell differentiation as demonstrated by impairment of Leydig cell development in Dhh −/− mice. Interestingly, PTM cell development is also compromised in Dhh −/− mice, and Dax1 −/− mice display similar impairment in both Leydig cells and PTM cells. Altogether, these results suggest that Leydig cells and PTM cells might differentiate from the same precursor cells, and reinforce the pivotal role of Sertoli cells in regulating the development of other cell lineages within the testis.

Which stimulates the testes to produce testosterone?

What hormone stimulates Leydig cells?

Does FSH or LH stimulate Leydig cells?

What is the pituitary hormone stimulates testosterone production in cells Leydig?