LH binds to Leydig cells and increases cAMP which increases protein secretion and the
side-chain cleavage of cholesterol, as well as other likely steps, to increase steroidogenesis
and the production of testosterone and other androgens. Regulated by steroid feedback.
The Leydig cells produce the testicular steroids, lie between the seminiferous tubules, and
assist in the transportation of steroids in the blood, lymph and seminiferous tubules.
FSH binds to the Sertoli cells of the seminiferous tubules, increases cAMP and protein
synthesis, androgen binding in the tubules, etc. Regulated by inhibin produced by the
Sertoli cells. Sertoli cells secrete proteins that are important to spermatogenesis and have
been called the director cells of spermatogenesis. They comprise the blood-testis barrier.
Prolactin may increase Leydig cell response to LH and/or prostate sensitivity to
Steroids and other hormones may aid in the movement of sperm from the testicle by
causing smooth muscle contractions.
Estradiol and dihydrotestosterone = extremely low in normal males.
Spermatogenesis occurs with the following steps:
Yolk sac endoderm gives rise to primordial germ cells which give rise to more type
A cells, some of which degenerate.
Type A stem cells form additional type A cells or differentiate into type B spermatogonia
cells during early puberty.
Type B cells differentiate during late puberty and in the adult to form primary
spermatocytes, secondary spermatocytes and spermatids. These events occur
initially through mitosis and then reduce the chromosomes to one-half through miosis.
Spermiogenesis transforms early spermatids into late spermatids and form what we
recognize as morphological normal sperm.
The above process takes 72 to 74 days in the human.
Sperm are released into the lumen through spermiogenesis which involves a gradual release
of sperm from the Sertoli cells into the tubule lumen.
Disorders of spermatogenesis can occur and can include:
Azoospermia including Sertoli cell only syndrome
Maturation arrest at one of a number of possible stages
Sperm transport from the testicle occurs through:
Seminiferous tubule contractions of the myoid cells (hormone dependent)
The history, physical exam, and laboratory investigations will detect an etiology for male factor infertility
in approximately 50% of cases. Serum FSH levels provide an important diagnostic parameter in
determining the pathological basis of azoospermia. Karyotypic analysis is most helpful in males with
azoospermia and small testes. Obstruction of the ejaculatory ducts can be diagnosed by ultrasound.
The absence of the vas deferens can be detected by the absence of fructose in the semen sample.
The most common congenital abnormality resulting in testicular dysfunction is cryptorchidism. *The
longer the testis remain outside the scrotum, the greater the degree of spermatic disruption. The most
common chromosomal abnormality resulting in deficient testicular function is Klinefelter's syndrome.
The frequency of this abnormality is 1 in
500 live births. The 47,XX7 karyotype results in the destruction of all germ cells with seminiferous
tubules causing small, firm testes and azoospermia. Gynecomastia and various degrees of androgen
deficiency are usually noted. The most common vascular abnormality associated with infertility is a
varicocele. The higher frequency of varicocele in infertile men (21% to 41%) compared to men in the
general population (4$ to 23%) has been interpreted as supporting a causal relationship between
varicocele and infertility. Theories to account for adverse testicular function with a varicocele include:
vascular stasis, back pressure, interference with oxygenation, reflux of renal or adrenal products into the
panipiniform plexus and interference with heat exchange function of the panipiniform plexus.