Hormonal control of Male Reproductive Functions

[Serotonin]

Welcome to class! I'm studying for my final in Human Physiology and one of the things I do is copy my notes to burn them into my brain. Since most of you use Testosterone and try to get your testicles working after a cycle I decided I'd share this with you guys if you feel like reading it!

Control of the Testes

In a normal adult man, the GnRH(gonadotropin releasing hormone) secreting neuroendocrine cells fire a brief burst of action potentials approximately every 90 min, secreting GnRH at these times. The GnRH reaching the anterior pituitary via the hypothalamo-pituitary portal vessels during each periodic pulse triggers the release of both Leutenizing Hormone (LH) and Follicle Stimulating Hormone (FSH) from the same cell type, although not necessarily in equal amounts. Thus, systemic plasma concentrations of FSH and LH also show pulsatility - rapid increases followed by slow decreases over the next 90 min or so as the hormones are slowly removed from the plasma.

There is a clear separation of the actions of FSH and LH within the testes. FSH acts on the Sertoli cells to stimulate the secretion of paracine agents needed for spermatogenesis. LH, by contrast, acts on the Leydig cells to stimulate testosterone secretion. In addition to its many important systemic effects as a hormone, the testosterone secreted by the Leydig cells also acts locally, as a paracrine agent, by moving from the interstitial spaces into the seminiferous tubules. Testoerone enters Sertoli cells, and it is via these cells that it facilitates spermatogenesis. Thus, despite the absence of a direct effect on cells in the seminiferous tubules, LH exerts an essential indirect effect because the testosterone secretion stimulated by LH is required for spermatogenesis!

The last components of the hypothalamo-pituitary control of malre reproduction that remain to be discussed are the negative feedback effects exerted by testicular hormones. Even though FSH and LH are prduced by the same cell type, their secretion rates can be altered to different degrees by negative feedback inputs.

Testosterone inhibits LH secretion in two ways: (1) it acts on the hypothalamus to decrease the amplitude of GnRH bursts, which results in a decrease in the secretion of gonadotropins; and (2) it acts directly on the anterior pituitary to cause less LH secretion in response to any given amount of GnRH.

How do the testes reduce FSH secretion? The major inhibitory signal, exerted directly on the anterior pituitary, is the protein hormone inhibin secreted by the Sertoli cells. This is a logical completion of a negative feedback loop such that FSH stimulates Sertoli cells to increase both spermatogeneis and inhibin production, and inhibin decreases FSH release.

Despite all of these complexities, the total amounts of GnRH, LH, FSH, testosterone, and inhibin secreted and of sperm produced are relatively constant from day to day in the adult male. This is completely different from the large cyclical variations of activity so characteristic of the female reproductive processes!

Testosterone!

In addition to its essential paracrine action within the testes on spermatogenesis and its negative feedback effects on the hypothalamus and anterior pituitary, testosterone exerts many other effects.

Some hormones must undergo transformation in their target cells in orer to be effective. This is true of testosterone in many (but not all) of its target cells. In some-for example, cells of the adult prostate- after its entry into the cytoplasm, testosterone is converted to dihydrotestosterone (DHT), which is more potent than testosterone. This conversion is catalyzed b the enzyme 5alpha-reductase, which is expressed in a wide variety of androgen target tissues. In certain other target cells (e.g., the brain), testosterone is transformed no to dihydrotestosterone but to estradiol (estrogen), which is the active hormone in these cells. The enzyme aromatase catalyzes this conversion. Note in this latter case that the "male" sex hormone must be converted to the "female" sex hormone to be active in the male. The fact that, ***ending on the target cells, testosterone may act as testosterone, DHT, or estradiol has important pathophysiological implications in since some men lack 5alpha-reductase or aromatase in some tissues. Therefore, they will exhibit certain signs of testosterone deficiency but not others.

Therapy for prostate cancer makes use of these facts: prostate cancer cells are stimulated by dihydrotestosterone, so the cancer can be trated with inhibitors of 5alpha-reductase. Furthermore, male pattern baldness may also be trated with 5alpha-reductase inhibitors, since DH tends to promote hair loss from the scalp.

Summary of effects of Testosterone in the Male

1. Required for initiation and maintenance of spermatogenesis.

2. Decreases GnRH secretion via an action on the hypothalamus.

3. Inhibits LH secretion via a direct action on the anterior pituitary.

4. Induces differentiation of male accessory reproductive organs and maintains their function.

5. Induces male secondary sex characteristics; opposes action of estrogen on breast growth.

6. Stimulates protein anabolism, bone growth, and cessation of bone growth.

7. Required for sex drive and may enhance aggressive behavior.

8. Stimulates erythropoietin secretion by the kidneys. (Red blood cell genesis)

Source: Vander's Human Physiology 10ed, 2006. McGraw Hill Higher Education
More to come!

[Lexed]

6. Stimulates protein anabolism, bone growth, and cessation of bone growth

how much does it increase it by I never noticed any bone growth gains

[Serotonin]

Well, that is the main reason men shouldn't take steroids until they're in their mid to late twenties and bone plates have fused.

Androgens stimulate bone growth, mostly through the stimulation of growth hormone secretion. Ultimately, however, androgens terminate bone growth by causing closure of the bones' epiphyseal plates.

[Lexed]

so your saying it could or could not increase bone growth?

[Serotonin]

It won't increase it after the bone plates have fused... and supplementing high levels of testosterone or HGH for that matter when you're bone plates have not fused can cause abnormal bone growths.

[Lexed]

so if our bones are not fused then it will make them grow but if there fused no way increase the growth. I made a thread before asking how to increase bone growth. Bigger bones= more weight/muscle

[novastepp]

Serotonin, i mentor your biology class

[Serotonin]

Yea, I thought about being and SI for organic chemistry and structure and function but the pay sucks major balls.

[Logan13]

so if our bones are not fused then it will make them grow but if there fused no way increase the growth. I made a thread before asking how to increase bone growth. Bigger bones= more weight/muscle

Estrogen causes the bone plates to close.

[Lexed]

so if you have proper pct and use anti estrogens during your cycle your bone plates wont fuse? I was at my doc month ago he said bone plates are still nto fused really dont want to fck t up