Follicle stimulating hormone (FSH
) is a
hormone synthesised and secreted by gonadotropes in the
anterior
pituitary gland. FSH and LH act synergistically in reproduction:
►In women, in the ovary FSH
stimulates the growth of immature Graafian follicles to maturation. As
the follicle grows it releases inhibin, which shuts off the FSH
production.
►In men, FSH enhances the production
of androgen-binding protein by the Sertoli cells of the testes and is
critical for spermatogenesis.
FSH is a glycoprotein. Each monomeric unit
is a protein molecule with a sugar attached to it; two of these make the
full, functional protein. Its structure is similar to LH, TSH, and hCG.
The protein dimer contains 2 polypeptide units, labelled alpha and beta
subunits. The alpha subunits of LH, FSH, TSH, and hCG are identical, and
contain 92 amino acids. The beta subunits vary.
FSH has a beta subunit of 118 amino acids (FSHB) that confers its
specific biologic action and is responsible for interaction with the
FSH-receptor.The sugar part of the hormone is composed of fucose,
galactose, mannose, galactosamine, glucosamine, and sialic acid, the
latter being critical for its biologic half-life. The half-life of FSH
is 3-4 hours.
The gene for the alpha subunit is located on chromosome
6p21.1-23. It is expressed in different cell types. The gene for the FSH
beta subunit is located on chromosome 11p13 and is expressed in
gonadotropes of the pituitary cells, controlled by GnRH, inhibited by
inhibin, and enhanced by activin.
Follicle-stimulating hormone (FSH) is a
glycoprotein gonadotropin secreted by the anterior pituitary in response
to gonadotropin-releasing hormone (GnRH), which is released by the
hypothalamus. The same pituitary cell also secretes luteinizing hormone
(LH), another gonadotropin. FSH and LH are composed of alpha and beta
subunits. The specific beta subunit confers the unique biologic
activity. FSH and LH bind to receptors in the testis and ovary and
regulate gonadal function by promoting sex steroid production and
gametogenesis.
In men, LH stimulates testosterone production from the interstitial
cells of the testes (Leydig cells). FSH stimulates testicular growth and
enhances the production of an androgen-binding protein by the Sertoli
cells, which are a component of the testicular tubule necessary for
sustaining the maturing sperm cell. This androgen-binding protein causes
high local concentrations of testosterone near the sperm, an essential
factor in the development of normal spermatogenesis. Sertoli cells,
under the influence of androgens, also secrete inhibin, a polypeptide,
which may help to locally regulate spermatogenesis. Hence, maturation of
spermatozoa requires both FSH and LH.
In women, LH stimulates estrogen and progesterone production from the
ovary. A surge of LH in the midmenstrual cycle is responsible for
ovulation, and continued LH secretion subsequently stimulates the corpus
luteum to produce progesterone. Development of the ovarian follicle is
largely under FSH control, and the secretion of estrogen from this
follicle is dependent on both FSH and LH. The granulosa cells of the
ovary secrete inhibin, which plays a role in cellular differentiation.
FSH and LH secretion are affected by a negative feedback from sex
steroids. Inhibin also has a negative feedback on FSH selectively.
High-dose testosterone or estrogen therapy suppresses FSH and LH.
Primary gonadal failure in men and women leads to high levels of both
FSH and LH, except in selective destruction of testicular tubules with
subsequent elevation of only FSH, as in Sertoli-cell-only syndrome.
Similarly, any process leading to a low FSH level also simultaneously
results in a low LH level, except in rare instances of isolated FSH
deficiency or isolated LH deficiency in fertile eunuch syndrome.
In both males and females, FSH stimulates the maturation of germ cells.
In females: FSH initiates the follicular growth, specifically affecting
granulosa cells. With the concomitant rise in inhibin B FSH levels then
decline in the late follicular phase. This seems to be critical in
selecting only the most advanced follicle to proceed to ovulation. At
the end of the luteal phase, there is a slight rise in FSH that seems to
be of importance to start the next ovulatory cycle.
Like its partner, LH, FSH release at the pituitary gland is controlled
by pulses of gonadotropin-releasing hormone (GnRH). Those pulses, in
turn, are subject to the estrogen feed-back from the gonads.
