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Women with PCOS often do not ovulate monthly due to low levels of the stimulating follicle.
Follicle-stimulating hormone (FSH), or follicle-stimulating hormone, is a hormone released by the pituitary gland in the brain that stimulates the growth of an egg follicle each month as part of the menstrual cycle.
If your doctor suspects you may have PCOS, they will order a follicle stimulating hormone blood test along with other hormone levels before diagnosis.
Older women tend to have elevated levels of follicle-stimulating hormone in the blood, indicating ovarian maturation . This is because higher amounts of the hormone are required for the ovary to recruit and stimulate an egg follicle.
FSH hormone functions
Follicle-stimulating hormone is necessary for the transition of secondary preantral follicles to the antral stage.
It is also a survival factor for antral follicles, and its removal triggers programmed cell death in the absence of local factors that sensitize the follicle to the action of the follicle-stimulating hormone or amplify its effects.
Follicular maturation initiated at the beginning of a new menstrual cycle is driven by increased levels of follicle-stimulating hormone in the late luteal phase as levels of progesterone, estradiol, and inhibin A decrease.
Preantral follicles apparently require a threshold level of follicle-stimulating hormone concentration to maintain growth, and this threshold level is reached during the late luteal phase.
Surprisingly, the threshold can be crossed with a 10% to 30% increase in follicle stimulating hormone, indicating that granulosa cells have a highly sensitive yet mysterious detection system with which they interpret circulating follicle hormone levels. stimulating.
Follicle stimulating hormone can induce follicular growth to the preovulatory size of at least 17 mm in the virtual absence of luteinizing hormone.
Although estradiol production is severely impaired under these circumstances, inhibin production is induced, reflecting the normal response of granulosa cells to follicle-stimulating hormone.
Granulosa cell division is promoted by follicle-stimulating hormone, possibly by an indirect mechanism.
This action is mediated by growth factors produced by somatic cells or the oocyte.
For example, in rodents, estrogens produced in response to follicle-stimulating hormone are an important mitogen for granulosa cells.
Follicle-stimulating hormone also increases the number of gap junctions, as well as the amount of binding membrane between granulosa cells.
An early sign that a dominant follicle has been selected is that its granulosa cells proliferate at a higher rate than cells in non-dominant follicles. Differential mitotic rates can be detected in the late follicular phase.
One of the main actions of follicle stimulating hormone is the induction of aromatase in granulosa cells.
Therefore, little or no estrogen can be produced by follicle-stimulating hormone unprimed granulosa cells, even if they are supplied with aromatizable androgen precursors.
Follicle stimulating hormone also induces the expression of cytochrome P450 reductase, which transfers electrons to aromatase, and by 17β-hydroxysteroid dehydrogenase type 1, “estrogenic” 17β-hydroxysteroid dehydrogenase, which reduces estrone to estradiol.
In vivo studies in rodents have shown that follicle stimulating hormone increases the number of its cognate receptors on granulosa cells.
In rodents, estrogens act synergistically with follicle-stimulating hormone in this regard, resulting in a feeding system that increases the responsiveness of follicle-stimulating hormone.
However, a similar advancement mechanism in primate follicle development has not yet been demonstrated.
Follicle-stimulating hormone induces luteinizing hormone receptors in the granulosa cells of the preovulatory follicle.
Consequently, in the later stages of follicular maturation, luteinizing hormone can fulfill the role of follicle-stimulating hormone in follicular maturation.
This attribute can allow the dominant follicle to complete its maturation cycle in the face of declining levels of follicle-stimulating hormone. In addition, the dominant follicle is primed to respond to increased ovulatory luteinizing hormone.
The follicle-stimulating hormone receptor is a seven-transmembrane G-protein-coupled receptor encoded by a single gene located on chromosome 2p21.
The primary signal transduction cascade initiated by the follicle-stimulating hormone receptor involves cyclic adenosine monophosphate.
However, increases in cyclic adenosine monophosphate alone evidently cannot replicate all the actions of follicle-stimulating hormone on granulosa cell function.
And alternative signaling pathways are activated by the follicle-stimulating hormone receptor (directly or indirectly), including mitogen-activated protein kinases and protein kinase B.
Some authors have identified follicle-stimulating hormone receptor variants that activate the calcium and protein kinase C signal transduction systems in the ovary.
Variants contain the receptor’s follicle-stimulating hormone-binding extracellular domain coupled to a single-pass growth factor-like membrane spanning domain.
However, its existence in the human ovary has yet to be verified, and its specific roles in follicle-stimulating hormone signaling have yet to be defined.
Importance
The importance of follicle-stimulating hormone in follicular development has been documented by the discovery of mutations that inactivate the β subunit of follicle-stimulating hormone and the follicle-stimulating hormone receptor in humans, and by specific deletions of these genes in mice.
Women who are homozygous for follicle-stimulating hormone receptor mutations have the characteristics of hypergonadotropic hypogonadism, with absent or poor development of secondary sexual characteristics and high levels of follicle-stimulating hormone and luteinizing hormone.
The ovarian phenotypes of humans with these mutations and those of follicle-stimulating hormone receptor and follicle-stimulating hormone β-subunit knockout mice are remarkably consistent.
In the absence of the functional follicle-stimulating hormone or follicle-stimulating hormone receptor subunit, the ovaries are small and follicular development generally does not go beyond the preantral stage.
The human genotype-phenotype correlation with follicle-stimulating hormone receptor mutations is reflected in the mouse inactivation model, in which follicle-stimulating hormone receptor haploinsufficiency accelerates oocyte loss and results in reproductive senescence. early.
Mutations in the transmembrane helices of the follicle-stimulating hormone receptor and the extracellular domain cause spontaneous ovarian hyperstimulation syndrome in which the ovaries overrespond to human chorionic gonadotropin.
Mutations in the transmembrane helices result in ligand promiscuity, allowing the receptor to respond to human chorionic gonadotropin and thyroid stimulating hormone.
Whereas mutations in the extracellular domain (S128Y) show greater specificity and sensitivity to human chorionic gonadotropin, but not to thyroid hormone stimulation.
FSH Hormone Levels During Your Cycle
Throughout your menstrual cycle, follicle-stimulating hormone levels vary. Doctors often test follicle-stimulating hormone levels on day 3 of your cycle. These are considered your reference levels.
Follicle-stimulating hormone is part of a complex dance of hormones that includes luteinizing hormone (LH), estradiol, and gonadotropin-releasing hormone (GnRH).
Follicle stimulating hormone stimulates the growth of an immature follicle. Once it’s grown, it releases estradiol, which signals the release of gonadotropin-releasing hormone and luteinizing hormone, causing ovulation.
Before ovulation, follicle stimulating hormone levels peak, signaling the ovary to release an egg.
Once ovulation has occurred, the levels return or drop slightly below the baseline. Normal basal levels are between 4.7 and 21.5 mIU / ml in menstruating women.
Certain medications, such as birth control pills, clomiphene, digitalis, and levodopa, can alter the test results. Your doctor will instruct you to stop taking these medications before taking a follicle-stimulating hormone test.
In the case of hormonal contraceptives, it should be stopped at least 4 weeks before the test.
Follicle Stimulating Hormone and Pregnancy Planning
Since women with PCOS have low levels of follicle-stimulating hormone and therefore do not ovulate regularly, she will usually see a fertility or reproductive endocrinology specialist for help in getting pregnant when the time is right. suitable.
Reproductive endocrinologists use a form of follicle-stimulating hormone to stimulate the ovaries and produce egg follicles for both IUI (intrauterine insemination) and IVF (in vitro fertilization).
These are injectable medications, more commonly known as Gonal-f, Follistim, and Bravelle.
Many women are often anxious to hear that they will need to take injections to stimulate ovulation. While injections can be uncomfortable, it’s important to keep your eye on the big picture – having a baby.
FSH hormone and ovarian reserve
In women who want to become pregnant later in life, follicle-stimulating hormone levels are used to assess ovarian reserve – the number of eggs a woman has left and the quality of the eggs.
Your doctor will do a blood test on the third day of your menstrual cycle. Results are generally available within 24 hours depending on the laboratory.
Basal levels of follicle-stimulating hormone increase as women enter perimenopause, indicating a decrease in the number of eggs that remain.
Perimenopause lasts 4 years on average and ends when a woman has not had a period in 12 months. At that point, menopause begins. Menopausal follicle-stimulating hormone levels are consistently elevated at 30 mIU / ml and above.
Follicle Stimulating Hormone and Puberty
Follicle-stimulating hormone is produced and exported from the pituitary to act primarily on Sertoli cells, although testicular interstitial macrophages may also respond.
Follicle stimulating hormone is a glycoprotein hormone that contains two subunits.
It is secreted in a pulsatile fashion in response to gonadotropin-releasing hormone (GnRH), also known as luteinizing hormone-releasing hormone (LHRH), from the hypothalamus .
Inhibin, secreted by the Sertoli cell, is believed to be involved in a feedback loop from the testis to the pituitary to inhibit follicle-stimulating hormone production.
Follicle-stimulating hormone is believed to exert most of its effects through a G-protein-coupled membrane receptor on Sertoli cells, which induces a classic cyclic adenosine monophosphate intracellular second-messenger response.
The action of follicle stimulating hormone in immature and mature animals is profoundly different.
Follicle-stimulating hormone is often considered to be the puberty hormone, as increased levels of follicle-stimulating hormone act as a trigger for testicular growth, junction formation between adjacent Sertoli cells, and secretion of androgen-binding proteins from the cells. Sertoli cells, and generally initiates spermatogenesis and the expansion of the seminiferous tubules.
Once this has occurred, the Sertoli cell changes its responsiveness from follicle-stimulating hormone to testosterone, since many of the functions regulated by follicle-stimulating hormone in the immature animal are absorbed by testosterone in the adult.
The impact and primary effects of follicle-stimulating hormone in the adult are poorly understood, although its importance appears to vary between species.
Suppression of follicle stimulating hormone in the adult rat has negligible effect on spermatogenesis, whereas in non-human primates it results in considerable suppression of spermatogenesis and sperm production.
In the rat, follicle-stimulating hormone appears to modify the number of differentiated spermatogonia that enter meiosis, but it has little effect on mitotic expansion of the undifferentiated and differentiating population.
In contrast, in primates, follicle-stimulating hormone appears to be important in regulating the expansion of undifferentiated stem cell spermatogonia, so alterations may have a much greater impact on spermatogenesis.
Follicle stimulating hormone appears to be the main regulatory hormone in seasonally reproducing animals, causing the Leydig cell population to expand and restarting spermatogenesis in response to a stimulating photoperiod.
Prolactin probably also plays an important role in these species by modifying the Leydig cell’s responsiveness to luteinizing hormone through altering the numbers of luteinizing hormone receptors.
Parts of the image were taken from the site https://www.reproduccionasistida.org
