Organ Systems Involved
The hypothalamic-pituitary-gonadal axis plays a major role in promoting sexual maturity, sperm production and the development of secondary sex characteristics. It maintains spermatogenesis and sexual function throughout the male’s lifetime. The hypothalamus secretes GnRH into the hypothalamo-hypophyseal portal system to stimulate the anterior pituitary. GnRH is a peptide hormone released by hypothalamic neurons in a pulsatile fashion. It acts on the gonadotrophs of the anterior pituitary via the binding and activation of a G protein receptor, which stimulates the anterior pituitary through inositol 1,4,5-triphosphate (IP3) activation (which increases intracellular calcium) to release FSH and LH. GnRH is inhibited by testosterone, estrogen, estradiol, and prolactin.[2]
In response, the anterior pituitary secretes LH and FSH into the blood. These gonadotropic hormones act on membrane receptors in the Leydig and Sertoli cells of the testes respectively. Both hormones come from the same glycoprotein family and consist of identical alpha subunits, but their different beta-subunit differentiates their functions. Both exert their physiologic effects by binding and activating a G protein receptor, which activates adenylyl cyclase and increases cellular cAMP levels, to stimulate Sertoli and Leydig cells. LH stimulates Leydig cells in the interstitium of the testes to produce testosterone from cholesterol. LH promotes desmolase, which is the initial rate-limiting enzyme that converts cholesterol into pregnenolone. This goes on to produce two key weak androgen intermediates: dehydroepiandrosterone (DHEA) and androstenedione. The enzyme 17-beta-hydroxysteroid dehydrogenase completes the conversion of androstenedione to testosterone. Testosterone acts on the hypothalamus and anterior pituitary via negative feedback to decrease the secretion of LH and FSH. Testosterone can also exert some effect on Sertoli cells, found in the periphery of the seminiferous tubules of testes. FSH and testosterone can stimulate Sertoli cells to release androgen-binding protein (ABP), which provides testosterone to germ cells during spermatogenesis. FSH stimulates Sertoli cells to promote sperm production and release inhibin B and MIS. Inhibin serves as the negative feedback control that Sertoli cells exert on the hypothalamic-pituitary system to decrease FSH release.[6]
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Before puberty, the levels of androgens and gonadotropins typically remain low and constant. Once puberty occurs, the hypothalamus releases GnRH in a pulsatile fashion every one to two hours to maintain amounts of FSH, LH and plasma testosterone, all of which regulate each other to maintain hormonal balance. In the third decade of life, testosterone levels are found to decline.[2][5][7]
Although a majority of testosterone production in men come from the Leydig cells in testes, the adrenal cortex contributes some androgen production. Similar to the hypothalamic-pituitary-gonadal axis, the adrenal glands are also controlled by the hypothalamus and anterior pituitary to form the hypothalamic-pituitary-adrenal axis. The hypothalamus release corticotrophin-releasing hormone (CRH), which stimulates the release of adrenocorticotropic hormone (ACTH) from the anterior pituitary. ACTH stimulates the enzyme desmolase to convert cholesterol into pregnenolone in the adrenals, similar to testosterone synthesis in the testes. Specifically, the zona reticularis of the adrenal medulla is responsible for generating the weak androgens DHEA and androstenedione, which go on to be converted to testosterone or estradiol peripherally.[2]
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