Estrogens

In addition to testosterone Leydig cells secrete small amounts of estradiol. Estradiol concentrations in the plasma of males are low compared with estradiol concentrations in the plasma of females. Progesterone concentrations in the plasma of males are low compared with progesterone concentrations in the plasma of females.

 

Testosterone

At about age 10 males begin to undergo puberty when the hypothalamic-pituitary unit begins to function like that of an adult. The hypothalamus begins to secrete increased amounts of gonadotropin-releasing hormone or GnRH in a pulse a pulsatile manner. The pituitary response to GnRH by secreting increased amounts of the gonadotropins, LH, and FSH in a pulsatile manner.

The gonads in turn respond to LH by secreting increased amounts of testosterone and to FSH by producing increased numbers of spermatozoa. The initial response of the gonads is termed gonadarche. However, the first recognizable hormonal change is an increase in adrenal androgen production termed as adrenarche. The transformation from an immature to mature state results from maturation of the neural mechanisms in the brain which regulate the pulsatile secretion of GnRH by the hypothalamus.

The neural mechanism is termed the GnRH pulse generator. The signal or signals responsible for maturation of the GnRH pulse generator have not been identified. Plasma testosterone concentrations in men increase on average from the thirties to the eighty's whereas plasma androstenedione concentrations declined steadily from the twenty's to the fifty's.

The first statistically significant decline in serum testosterone around does not occur until men reach their eighty's except in the cases of testicular pathology. The rise in plasma dihydrotestosterone concentrations between ages 60 and 80 may be responsible for prosthetic hyperplasia in aging men. Testosterone has dramatic effects on multiple tissues in both males and females.

First, it stimulates the differentiation of the male reproductive tract and brain during fetal development. Second, it stimulates maturation of the external genitalia at puberty. Third, it increases the size of the larynx and the thickness of the vocal cords of puberty. Fourth, it increases the growth of facial axillary and pubic hair as well as hair recession or balding.

Fifth, it increases sexual drive or libido sexual potency and aggressive behavior. Sixth it maintains the male reproductive tract and sex accessory glands. Seventh, it maintains spermatogenesis in conjunction with FSH. Eighth, It decreases LH and to a lesser extent, FSH secretion by decreasing GnRH secretion. Ninth, it stimulates bone growth and closure of the epiphyses at puberty.

Tenth, it increases protein anabolism both by increasing protein synthesis and by decreasing protein breakdown, leading to increased linear body growth, nitrogen retention, and muscular development. Finally testosterone increases the risk erythropoiesis by increasing renal erythropoietin production resulting in a proliferation of erythroid stem cells and the higher homacid observed in men compared to women.

 

Gonadotropins/hCG

FSH and LH increase markedly in the fetal circulation in both males and females around the middle of gestation and then decline. FSH and LH are secreted by the fetal pituitary in response to GnRH secreted by the fetal hypothalamus. The bell-shaped time course of gonadotropin secretion during gestation reflects the activity of the fetal hypothalamus-pituitary unit before the hypothalamic-pituitary unit becomes sensitive to the negative feedback effects of sex steroids.

Gonadotropin levels in infantile males and females are elevated by the sudden absence of the inhibitory effect of placental steroids. During childhood gonadotropin levels are low but the pituitary is responsive to exogenous GnRH. Pre-pubertal males and females secrete gonadotropins in response to GnRH although females are more sensitive. During adulthood the Leydig cells respond to LH which binds to the same receptors as HCG.

The Leydig cells disappeared during childhood because there is no HCG or LH. They do not reappear until puberty when plasma levels of LH increase and they are maintained by LH. In addition to stimulating general functions of the Leydig cells LH stimulates the synthesis of steroid acute regulatory protein or STAR.

STAR facilitates the transport of cholesterol from the outer mitochondrial membrane of Leydig cells resulting in increased steroid biosynthesis. In the 7th week of gestation and response to the placental human chorionic gonadotropin or HCG, testicular Leydig cells differentiate, proliferate and begin to secrete androgens. During adulthood they respond to LH which binds to the same receptors as HCG.

Most leydig cells disappear during childhood due to the low levels of LH in plasma and they do not reappear until puberty when plasma levels of LH increase.