The role of HCG in sperm production as an LH analog

[Guest guest]

Here is one of the best explinations to how HCG works in fertility treatment.

As an LH

analog it works similar to LH in LH receptors found in the lydig cells.

Hormonal Control of Spermatogenesis

An intimate structural and functional relationship exists between the two

separate

compartments of the testis, i.e. the seminiferous tubule and the interstitium

between the

tubules. LH effects spermatogenesis indirectly in that it stimulates androgenous

testosterone production. FSH targets Sertoli cells. Therefore, testosterone and

FSH are the

hormones that are directed at the seminiferous tubule epithelium.

Androgen-binding

protein which is a Sertoli cell product carries testosterone intracellularly and

may serve as

a testosterone reservoir within the seminiferous tubules in addition to

transporting

testosterone from the testis into the epididymal tubule. The physical proximity

of the

Leydig cells to the seminiferous tubules and the elaboration by the Sertoli

cells of

androgen-binding protein, cause a high level of testosterone to be maintained in

the

microenvironment of the developing spermatozoa. The hormonal requirements for

initiation of spermatogenesis appear to be independent of the maintenance of

spermatogenesis. For spermatogenesis to be maintained like for instance after a

pituitary

obliteration, only testosterone is required. However, if spermatogenesis is to

be re-

initiated after the germinal epithelium has been allowed to regress completely,

then both

FSH and testosterone are required.

Endocrine Therapy

Infertile men with hypogonadotropic hypogonadism (secondary hypogonadism) are

the

only appropriate candidates for exogenous gonadotropin therapy. For initiation

of

spermatogenesis, LH must be given to stimulate the Leydig cells to produce high

intratesticular testosterone levels. hCG (Pregnyl or Profasi) 2,000 IU

intramuscularly three

times a week is usually effective in stimulating adequate production of

testosterone for full

virilization. Once the patient is fully virilized and 8-12 months of hCG therapy

have not led

to the production of sperm, then FSH therapy should be initiated. FSH is

available as

human menopausal gonadotropin (hMG). The commercial preparation Pergonal

contains

75 IU of FSH and 75 IU of LH per vial. The usual dosage is 1/2 to 1 vial

intramuscularly

three times weekly. Since hCG and hMG are compatible in solution, the same

syringe may

be used. It takes months for sperm to appear in the ejaculate after initiation

of FSH

therapy. With the normal response, most patients achieve a sperm count of

between 2 and

5 million sperm per ejaculate and then impregnation is possible. Once a

pregnancy has

occurred, the FSH therapy can be stopped. Spermatogenesis can be maintained with

hCG

alone. An alternative to exogenous gonadotropin usage is the use of GnRH to

stimulate LH

and FSH endogenously. GnRH must be given in a pulsatile manner as continuous

administration down-regulates the pituitary. The initial dosage is 25-50

ng/kilogram

every two hours by a small infusion pump. Both the gonadotropins and GnRH are

expensive. Although GnRH achieves a more physiologic pattern of gonadotropin

stimulation, its superiority has yet to be proved. Pituitary disease is not

amenable to GnRH

therapy, and combined treatment with hCG and hMG will be necessary. Individuals

with the

fertile eunuch syndrome (partial LH deficiency) may respond to hCG therapy

alone.

http://www.ivf.com/shaban.html

For a graphical representation, please see the following documents and graphics

/files/

Reproductive%20Endocrinology%20/

Testosterone, DHT, and estradiol

Regarding the two negative feedback loops for LH and FSH

Testosterone, DHT, and estradiol provide negative feedback on the

hypothalamic-pituitary

axis. In males, estradiol is the main inhibitor of LH production, whereas both

estradiol

and inhibin B, a peptide produced by Sertoli cells of the testes, inhibit

production of FSH.

In the presence of testosterone, FSH stimulates the Sertoli cells and induces

spermatogenesis. In spermatogenesis, each germinal cell (spermatogonium),

located

adjacent to the Sertoli cells, undergoes differentiation into 16 primary

spermatocytes, each

of which generates 4 spermatids. Each spermatid matures into a spermatozoon.

Spermatogenesis takes 72 to 74 days and yields about 100 million new spermatozoa

each

day. Upon maturation, spermatozoa are released into the rete testis, where they

migrate to

the epididymis and eventually to the vas deferens. Migration requires an

additional 14

days. Before ejaculation, spermatozoa are mixed with secretions from the seminal

vesicles,

prostate, and bulbourethral glands.

http://www.merck.com/mmpe/sec17/ch227/ch227a.html

[Guest guest]

Sorry if I'm a little testy on this point, but after reading all

kinds of conflicting information from various web sites,

I've come to trust only peer reviewed publications and

actual medical manuals.

I really don't think you can get an unbiased opinion of Clomid

from http://www.clomid.havingbabies.com/

Nor do I think you will get unbiased information about drugs

manufactured by merck from merck.com.

Yes, HCG is an LH analog. It is the first line treatment for

infertile men. This information comes from a peer

reviewed non-biased, not influenced by any particular

drug manufacturer, publication.

Sertoli Cell Biology By K. Skinner, D. Griswold

Page 185

" Conventionally, gonadotropin treatment in infertile

hypogonadotropic men is based on a treatment starting

with hCG, a naturally long-acting analog of LH. FSH is usually

added to the treatment regimen if sperm production does

not appear withing 6 months of hCG treatment. "

FSH is only added if spermatogenesis has not been achieved

within 6 months.

The description below is describes spermatogenesis in non-

hypogonadal men, but that's not what we are talking about.

We are talking about restarting spermatogenesis in hypogonadal

men that have suppressed or inadequate HPTA function.

The book reference above has a lot of good info about male

fertility. I'm just don't want to post too much from it in one

thread due to copy right considerations.

>

> Here is one of the best explinations to how HCG works in fertility treatment.

As an LH

> analog it works similar to LH in LH receptors found in the lydig cells.

>

> Hormonal Control of Spermatogenesis

>

> An intimate structural and functional relationship exists between the two

separate

> compartments of the testis, i.e. the seminiferous tubule and the interstitium

between

the

> tubules. LH effects spermatogenesis indirectly in that it stimulates

androgenous

> testosterone production. FSH targets Sertoli cells. Therefore, testosterone

and FSH are

the

> hormones that are directed at the seminiferous tubule epithelium.

Androgen-binding

> protein which is a Sertoli cell product carries testosterone intracellularly

and may serve

as

> a testosterone reservoir within the seminiferous tubules in addition to

transporting

> testosterone from the testis into the epididymal tubule. The physical

proximity of the

> Leydig cells to the seminiferous tubules and the elaboration by the Sertoli

cells of

> androgen-binding protein, cause a high level of testosterone to be maintained

in the

> microenvironment of the developing spermatozoa. The hormonal requirements for

> initiation of spermatogenesis appear to be independent of the maintenance of

> spermatogenesis. For spermatogenesis to be maintained like for instance after

a

pituitary

> obliteration, only testosterone is required. However, if spermatogenesis is to

be re-

> initiated after the germinal epithelium has been allowed to regress

completely, then

both

> FSH and testosterone are required.

>

>

> Endocrine Therapy

>

> Infertile men with hypogonadotropic hypogonadism (secondary hypogonadism) are

the

> only appropriate candidates for exogenous gonadotropin therapy. For initiation

of

> spermatogenesis, LH must be given to stimulate the Leydig cells to produce

high

> intratesticular testosterone levels. hCG (Pregnyl or Profasi) 2,000 IU

intramuscularly

three

> times a week is usually effective in stimulating adequate production of

testosterone for

full

> virilization. Once the patient is fully virilized and 8-12 months of hCG

therapy have not

led

> to the production of sperm, then FSH therapy should be initiated. FSH is

available as

> human menopausal gonadotropin (hMG). The commercial preparation Pergonal

contains

> 75 IU of FSH and 75 IU of LH per vial. The usual dosage is 1/2 to 1 vial

intramuscularly

> three times weekly. Since hCG and hMG are compatible in solution, the same

syringe

may

> be used. It takes months for sperm to appear in the ejaculate after initiation

of FSH

> therapy. With the normal response, most patients achieve a sperm count of

between 2

and

> 5 million sperm per ejaculate and then impregnation is possible. Once a

pregnancy has

> occurred, the FSH therapy can be stopped. Spermatogenesis can be maintained

with

hCG

> alone. An alternative to exogenous gonadotropin usage is the use of GnRH to

stimulate

LH

> and FSH endogenously. GnRH must be given in a pulsatile manner as continuous

> administration down-regulates the pituitary. The initial dosage is 25-50

ng/kilogram

> every two hours by a small infusion pump. Both the gonadotropins and GnRH are

> expensive. Although GnRH achieves a more physiologic pattern of gonadotropin

> stimulation, its superiority has yet to be proved. Pituitary disease is not

amenable to

GnRH

> therapy, and combined treatment with hCG and hMG will be necessary.

Individuals with

the

> fertile eunuch syndrome (partial LH deficiency) may respond to hCG therapy

alone.

>

> http://www.ivf.com/shaban.html

>

> For a graphical representation, please see the following documents and

graphics

>

> /files/

> Reproductive%20Endocrinology%20/

> Testosterone, DHT, and estradiol

>

> Regarding the two negative feedback loops for LH and FSH

>

> Testosterone, DHT, and estradiol provide negative feedback on the

hypothalamic-

pituitary

> axis. In males, estradiol is the main inhibitor of LH production, whereas both

estradiol

> and inhibin B, a peptide produced by Sertoli cells of the testes, inhibit

production of

FSH.

>

> In the presence of testosterone, FSH stimulates the Sertoli cells and induces

> spermatogenesis. In spermatogenesis, each germinal cell (spermatogonium),

located

> adjacent to the Sertoli cells, undergoes differentiation into 16 primary

spermatocytes,

each

> of which generates 4 spermatids. Each spermatid matures into a spermatozoon.

> Spermatogenesis takes 72 to 74 days and yields about 100 million new

spermatozoa

each

> day. Upon maturation, spermatozoa are released into the rete testis, where

they migrate

to

> the epididymis and eventually to the vas deferens. Migration requires an

additional 14

> days. Before ejaculation, spermatozoa are mixed with secretions from the

seminal

vesicles,

> prostate, and bulbourethral glands.

>

> http://www.merck.com/mmpe/sec17/ch227/ch227a.html

>