The Hormonal Control of Spermatogenesis

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Spermatogenesis is defined as the process of development of the sperm cell. The process occurs in the seminiferous tubules. It entails two processes: mitosis and meiosis. A number of stages are involved, and its aim is the production of four haploid sperm cells from the diploid spermatogonium. Mitosis acts as a replication phase while meiosis is the reduction phase and each of them has divisions namely: interphase, prophase, metaphase, anaphase and telophase. Several factors are crucial in the regulation of spermatogenesis. They include hormones, temperature and the blood-testis barrier which has a number of functions.

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Hormones Involved in Spermatogenesis

Spermatogenesis has less or no reliance on the germ cell but is rather dependent on the hormonal action on Sertoli cells and the interactions between the germ cells and the Sertoli cells. Sperm production is driven and controlled by hormones. It comprises hormones from the brain. The hormones play a role in this process, and they entail a control system. They include Follicle Stimulating Hormone, Luteinizing Hormone, testosterone and hormone inhibin involved in the negative feedback mechanism. Some act as agonists while others act synergistically.

Follicle Stimulating Hormone

The gonadotropin-releasing hormone (GnRH) plays a key role in the release of the FSH hormone. It stimulates the anterior pituitary gland via the hypophyseal portal vessels that lead to the release of both the Follicle Stimulating Hormone and Luteinizing Hormone. The Follicle Stimulating Hormone stimulates the process of spermatogenesis. It works by binding to its receptor on Sertoli cells and spermatogonia. Owing to the Sertoli cells being the only cells with FSH receptor, the hormone acts on it directly. It works via the cyclic AMP pump.It then enters the testes and acts by stimulating the Sertoli cells and formation of a blood-testis barrier. The Sertoli cells, in turn, provide nourishment to the sperm cells produced by the testes and thus facilitates spermatogenesis. Addition to this is that the Follicle Stimulating Hormone initiates sequestration of testosterone. It has been noted that an increase in the FSH levels results in an increment in the production of spermatozoa. This is possible as type A spermatogonia are not apoptosed. The hormone suppresses the proapoptotic signals and, therefore, promotes spermatogenesis.

Luteinizing Hormone

It is released by the action of the gonadotropin releasing hormone on the anterior pituitary gland. The LH produced enters testes and acts on the interstitial cells also called Leydig cells to release hormone testosterone into blood and testes. It plays a crucial role in the stimulation of spermatogenesis. It is also responsible for androgen production through stimulation of testes. It suppresses the proapoptotic signals and thus promotes survival of spermatogenic cells. A precise analysis of the action of the hormone is that increase in its levels results in an increment in the testosterone level, and subsequently, it inhibits the production of the gonadotropin-releasing hormone. This, therefore, ensures that testosterone levels are maintained.

Figure 1


Not only is the hormone involved in the development of sexual characteristics but also it plays a role in stimulation of spermatogenesis. The Luteinizing Hormone acts on Leydig cells and thus stimulates testosterone production. It acts as a negative feedback mechanism and inhibits the gonadotropin releasing hormone.. This means that presence of testosterone results in less Follicle Stimulating Hormone required for spermatogenesis. The action of testosterone on spermatogenesis involves the regulation of Sertoli cells. It acts on Sertoli cells and the peritubular myoid cells and has been noted that the cells mediate the process of spermatogenesis as the germ cells cant express the receptors such as those of androgen. The absence of the hormone will result in no transition between steps 7 and 8 of spermatogenesis. This means the elongation process cant be completed. It has also been noted that lowering the intratesticular testosterone in experiments resulted in the apoptotic death of germ cells.


The hormone is part of the feedback mechanism that controls the production of FSH. It is produced by Sertoli cells when sperm count gets to higher levels. It is a glycoprotein that inhibits the gonadotropin releasing hormone and, as a result, secretion of the FSH and LH which play a fundamental role in spermatogenesis are hindered. This, therefore, causes spermatogenesis to slow down. A decrease in sperm count to 20 million/ml triggers the Sertoli cells to stop the release of the hormone and spermatogenesis increases for more sperm count. Experiments with mice showed that testes injected with inhibin resulted in a notable decrease in the number of spermatogonia.

Figure 2

Epidermal Growth Factor

Experiments and research done on the mice showed that they produced the EGF in high amounts, and it was noted that it had a role in spermatogenesis. It was produced by the submandibular gland and on removal, there was impairment in the process of sperm formation. A substitute for it resulted in normal spermatogenesis. This concludes that Epidermal Growth Factor plays a significant role in the process and that its levels should always be maintained.

In conclusion, the actions of the different hormones cannot be overemphasized. Without spermatogenesis life would most likely come to an end. The formation of sperms and proper maturation requires a number of factors. Hormones, as seen above, play a crucial role. Another factor like temperature is essential. Since the major components are proteins, it is very likely that above a certain temperature denaturing occurs. The role of hormones in spermatogenesis has been applied in a number of fields. Pharmacologically and genetically we can point out the role of FSH in stimulation of the Sertoli cells. This is usually in the prepubertal development. Today the men with suppressed gonadotropin can have spermatogenesis through the use of FSH. Further studies have established that testosterone treatment is possible for those lacking FSH and LH as a result of the failure of activation of gonadotropin releasing hormone locus.

Reference List

Handelsman, D. (2010). 020. HORMONAL REGULATION OF SPERMATOGENESIS. Reprod. Fertil. Dev., 22(9), p.8.

Pfaff, D. (2002). Hormones, brain, and behavior. Amsterdam: Academic Press.

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