Leydig cells represent the endocrine proportion of the testis. In all mammalian males, Leydig cells are the main site of testosterone synthesis and secretion and are, thus, essential for male reproductive function. Developmentally, human Leydig cells appear in three separate stages: fetal, neonatal, and pubertal. Each of these stages underlies a corresponding epoch of testosterone secretion in the male lifespan.

Testosterone is synthesized from cholesterol in a series of reactions catalyzed by four enzymes. The first enzyme, P450scc, converts cholesterol to pregnenolone and is located in the inner mitochondrial membrane. Therefore, movement of cholesterol from the Leydig cell cytosol into the mitochondria is the rate-limiting step and is performed by the carrier proteins StAR and PBR. The three other biosynthetic enzymes, 3P-HSD, P45017a, and 17P-HSD, are situated in the SER. Testosterone can be metabolized into other steroids, DHT and E2, primarily by two enzymes: 5a-reductase and P450arom. The A5 and A4 steroidogenic pathways are followed in Leydig cells, with one preferred over the other depending on the species and developmental status. In humans, the A5 pathway from 17a-hydroxypregnenolone to dehydroepiandrosterone is predominant.

Development of steroidogenesis in Leydig cells is regulated by the pituitary gonadotropic hormone LH. FSH and cell-cell interactions in the testis also participate in this regulatory process. Decreased numbers and atrophy of cytological structure, as well as reduced steroidogenic ability, occur during Leydig cell aging, lowering testosterone secretion in older men. LCTs have a low incidence in humans, constituting only 1-3% of testicular neoplasms, with the highest incidence being for men in their 50s. Because testosterone is necessary for spermatogenesis, Leydig cells are a target for male hormonal contraception. Control of male fertility through suppression of Leydig cells will require identifying a level of intratesticular androgen concentration that is sufficient for spermatogenesis while maintaining libido and skeletal muscle mass in the periphery. Studies of reproductive toxicants have shown that disruption of Leydig cell steroidogenic function cannot be ignored as a causative factor.

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