Hormones of MaleReproduction

Endocrine Regulationof Testicular Function

Follicle-stimulating hormone (FSH) and luteinizinghormone (LH), protein hormones (see Chapter 12) from
the adenohypophysis (anterior
pituitary), are the primary endocrine regulators
of testicular function. Their overall effect
is to stimulate testicular function, so both are
considered to be gonadotrophins. FSH promotes
spermatogenesis by its actions on the
germ cells in the seminiferous tubules and the
sustentacular cells that support the development
of the spermatozoa. LH acts on testicular
interstitial cells to promote the secretion of
androgens, primarily testosterone. The testosterone
produced by the interstitial cells is necessary
for the completion of spermatogenesis,
so both FSH and LH are required for normal
spermatogenesis.
A single hormone from the hypothalamus,
gonadotrophin-releasing hormone (GnRH),
stimulates the release of both FSH and LH from
the adenohypophysis. Negative feedback to the
hypothalamus to regulate GnRH is provided by
serum testosterone, which is produced by testicular
interstitial cells when stimulated by LH.
Testosterone also has direct effects on the adenohypophysis
to suppress LH release directly.
When stimulated by FSH, sustentacular cells
produce a protein hormone, inhibin. Inhibin
has a negative feedback effect on the adenohypophysis
to suppress further releases of FSH.
In farm animals, the feedback regulation of
GnRH, FSH, and LH secretion is such that spermatogenesis
is maintained at rates adequate for
breeding throughout the year. However, plasma
levels of FSH, LH, and testosterone do vary
with season in some species, and these have
been associated with differences in sexual activity.
For example, FSH, LH, and testosterone
levels are highest in rams while the days are
getting shorter, and this is associated with
increased sexual activity.
Follicle-stimulating hormone (FSH) and luteinizing
hormone (LH), protein hormones (see
Chapter 12) from the adenohypophysis (anterior
pituitary), are the primary endocrine regulators
of testicular function. Their overall effect
is to stimulate testicular function, so both are
considered to be gonadotrophins. FSH promotes
spermatogenesis by its actions on the
germ cells in the seminiferous tubules and the
sustentacular cells that support the development
of the spermatozoa. LH acts on testicular
interstitial cells to promote the secretion of
androgens, primarily testosterone. The testosterone
produced by the interstitial cells is necessary
for the completion of spermatogenesis,
so both FSH and LH are required for normal
spermatogenesis.
A single hormone from the hypothalamus,
gonadotrophin-releasing hormone (GnRH),
stimulates the release of both FSH and LH from
the adenohypophysis. Negative feedback to the
hypothalamus to regulate GnRH is provided by
serum testosterone, which is produced by testicular
interstitial cells when stimulated by LH.
Testosterone also has direct effects on the adenohypophysis
to suppress LH release directly.
When stimulated by FSH, sustentacular cells
produce a protein hormone, inhibin. Inhibin
has a negative feedback effect on the adenohypophysis
to suppress further releases of FSH.
In farm animals, the feedback regulation of
GnRH, FSH, and LH secretion is such that spermatogenesis
is maintained at rates adequate for
breeding throughout the year. However, plasma
levels of FSH, LH, and testosterone do vary
with season in some species, and these have
been associated with differences in sexual activity.
For example, FSH, LH, and testosterone
levels are highest in rams while the days are
getting shorter, and this is associated with
increased sexual activity.

Testosterone and Its Effects

Testosterone is a steroid hormone that enters its
target cells to exert its effects. Within target
cells, testosterone is converted to dihydrotesterone,
which binds to intracellular receptors. In
addition to supporting the maturation of spermatozoa
within the testis, testosterone promotes
the development and function of male
accessory sex organs, causes development of
secondary sex characteristics, and promotes
male sexual behavior.
Lack of libido (sex drive) and inability to
produce offspring are two of the most obvious
effects of castration and the resultant lack of
testosterone. However, animals castrated after
attaining sexual maturity may continue to mate
for some time if they had sexual experience
before castration. If an animal is castrated
before puberty, many of the masculine secondary
sex characteristics fail to develop, and the
castrated animal tends to resemble the female
of the species. In addition, the accessory sex
glands fail to develop normally if castration
occurs early in life, and they regress and become
nonfunctional if castration occurs after sexual
maturity. Even though testosterone production
by the testis is necessary for a normal libido, it
is not testosterone that directly affects neurons
within the brain to produce a normal libido.
Within neurons, testosterone is converted to
estradiol, an estrogen, and it is this estradiol
that actually stimulates the appropriate neurons.
Anabolic steroids (discussed next) used to
promote growth cannot be converted to estradiol
and thus these do not increase the libido.
Anabolic steroids are synthetic compounds
used to increase net protein synthesis
and skeletal muscle mass. In this manner,
these compounds are similar to endogenous
androgens such as testosterone. Because of
their similarity to testosterone and endogenous
androgens, anabolic steroids also
promote the development of secondary
sexual characteristics and exert a negative
feedback effect on the hypothalamic–pituitary
axis. As a result of this negative feedback,
endogenous testosterone production
and spermatogenesis are suppressed. It is
not clear whether these can return to normal
levels if animals receive anabolic steroids
for prolonged periods.