Luteinizing hormone

Released from the pituitary and stimulates testosterone production in the testes.



Luteinizing hormone (LH) is a hormone produced by gonadotropic cells in the anterior pituitary gland. 



An acute rise of LH triggers ovulation in females and development of the corpus luteum. 



In males, LH had also been called interstitial cell–stimulating hormone (ICSH).



LH stimulates Leydig cell production of testosterone.


Stimulates follicular maturation and ovulation in women; or testosterone production and spermatogenesis in men.



It acts synergistically with follicle-stimulating hormone (FSH).



LH is a heterodimeric glycoprotein. 



One alpha and one beta subunit make the full, functional protein, similar to that of the other glycoprotein hormones, follicle-stimulating hormone (FSH), thyroid-stimulating hormone (TSH), and human chorionic gonadotropin (hCG). 



The alpha subunits of LH, FSH, TSH, and hCG are identical, and contain 92 amino acids.



The beta subunits of LH has a beta subunit of 120 amino acids that confers its specific biologic action and is responsible for the specificity of the interaction with the LH receptor. 



The biologic half-life of LH is 20 minutes.



FSH half life 3–4 hours and hCG 24 hours.



The biological half-life of LH is 23 hours subcutaneous or terminal half life of 10-12 hours.



The gene for the alpha subunit is located on chromosome 6q12.21



The luteinizing hormone beta subunit gene is localized in the LHB/CGB gene cluster on chromosome 19q13.32. 



LH is regulated by the gonadotropin-releasing hormone from the hypothalamus. 



LH works in males and females on endocrine cells in the gonads to produce androgens.



It supports theca cells in the ovaries that provide androgens and hormonal precursors for estradiol production. 



Menstruation: FSH initiates follicular growth, specifically affecting granulosa cells.



As estrogens rise, LH receptors are also expressed on the maturing follicle, which causes it to produce more estradiol. 



When the follicle has fully matured, a spike in 17α-hydroxyprogesterone production by the follicle inhibits the production of estrogens, leading to a decrease in estrogen-mediated negative feedback of GnRH in the hypothalamus, which then stimulates the release of LH from the anterior pituitary.



The increase in LH production only lasts for 24 to 48 hours, and triggers ovulation, releasing the egg from the follicle, initiating the conversion of the residual follicle into a corpus luteum that, in turn, produces progesterone to prepare the endometrium for a possible implantation. 



LH is necessary to maintain luteal function for the second two weeks of the menstrual cycle. 



If a pregnancy occurs, LH levels decrease.



With pregnancy  luteal function is maintained by the action of hCG, a hormone very similar to LH but secreted from the new placenta.



The gonadal steroids estrogens and androgens have negative feedback effects on GnRH-1 release at the level of the hypothalamus and at the gonadotropes, reducing their sensitivity to GnRH. 



Positive feedback by estrogens occurs in the gonadal axis and is responsible for the midcycle surge of LH that stimulates ovulation. 



Rupture of the ovarian follicle at ovulation causes a drastic reduction in estrogen synthesis and a marked increase in secretion of progesterone by the corpus luteum in the ovary, promoting a predominantly negative feedback on hypothalamic secretion of GnRH-1.



LH acts upon the Leydig cells of the testis and is regulated by gonadotropin-releasing hormone (GnRH).



The Leydig cells produce testosterone under the control of LH.



LH regulates the expression of the enzyme 17β-hydroxysteroid dehydrogenase that is used to convert androstenedione, the hormone produced by the testes, to testosterone. 



The onset of puberty in males is controlled by two major hormones: FSH initiates spermatogenesis and LH signals the release of testosterone.



Testosterone, an androgen that exerts both endocrine activity and intratesticular activity on spermatogenesis.



LH is released from the pituitary gland.



LH release  is controlled by pulses of gonadotropin-releasing hormone. 



When blood testosterone levels are low, the pituitary gland is stimulated to release LH.



As the levels of testosterone rise, it will act on the pituitary gland as a negative feedback loop and inhibit the release of GnRH and LH consequently.



Androgens that include testosterone and dihydrotestosterone inhibit monoamine oxidase (MAO) in the pineal gland, leading to increased melatonin and reduced LH and FSH by melatonin-induced increase of Gonadotropin-Inhibitory Hormone (GnIH) synthesis and secretion. 



Testosterone can also be changed  into estradiol to inhibit LH. 



Estradiol decreases pulse amplitude and responsiveness to GnRH from the hypothalamus onto the pituitary.



Changes in LH and testosterone blood levels and pulse secretions are induced by changes in sexual arousal in human males.



LH levels are normally low during childhood and, in women, high after menopause. 



LH is secreted as pulses.



During the reproductive years, typical levels are between 1–20 IU/L. 



High LH levels are seen during the LH surge.



Surges in LH levels typically last 48 hours.



In males over 18 years of age, ranges have been estimated to be 1.8–8.6 IU/L.



Luteinizing hormone surges in women indicates impending ovulation. 



LH can be detected by urinary ovulation predictor kits.



These tests  are performed, typically daily, around the time ovulation may be expected.



Conversion of the test from negative to a positive reading would suggest that ovulation is about to occur within 24–48 hours, giving women two days to engage in sexual intercourse or artificial insemination with the intention of conceiving.



Relatively elevated LH is frequently seen in patients with polycystic ovary syndrome.



Persistently high LH levels are indicate  normal restricting feedback from the gonad is absent. manifesting as pituitary production of both LH and FSH.



Persistently high LH levels is typical in menopause.



Diminished secretion of LH can result in failure of gonadal function.



 Diminished secretion of LH typically manifests in males as failure in production of normal numbers of sperm. 



Diminished secretion of LH typically manifests in females, amenorrhea is commonly observed. 



Conditions with very low LH secretions include:



Pasqualini syndrome



Kallmann syndrome



Hypothalamic suppression






Eating disorder



Female athlete triad









Gonadal suppression therapy



GnRH antagonist



GnRH agonist inducing an initial stimulation followed by permanent blockage of the GnRH pituitary receptor.



LH is available mixed with FSH in the form of menotropin.



Urinary gonadotropins may reduce the LH portion in relation to FSH. 



Recombinant LH is available as lutropin alfa (Luveris).



These medications have to be given parenterally, and are commonly used in infertility therapy to stimulate follicular development.


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