Luteinizing hormone – Role of LH in male
and female Reproductive System – LH
Related Diseases
If you are searching about Luteinizing hormone (LH) then, you are at your best place
in this regard. Let’s have a look at Role of LH in male and female Reproductive
System and LH Related Diseases:
What is a hormone?
The hormone can be regarded as messenger molecules. They are chemical
substances that travel in the body to control the cells and organs to do their work.
Hormones heavily control the human body’s reproductive system, and the luteinizing
hormone is one of those hormones. With different roles in the bodies of men and
women, this important hormone is crucial to ensuring a healthy reproductive system.
Taking control of your reproductive health requires understanding this essential
hormone.
What is the Luteinizing hormone (LH)?
Luteinizing hormone (LH) is produced and released in the anterior pituitary gland.
This hormone is considered a gonadotrophic hormone because of its role in
controlling the function of ovaries in females and testes in males, which are known as
gonads. [1] Luteinizing hormone (LH) is a glycoprotein hormone co-secreted along
with follicle-stimulating hormone by the gonadotrophin cells in the adenohypophysis
(anterior pituitary). Luteinizing hormone is a part of a neurological pathway
comprised of the hypothalamus, the pituitary gland, and gonads. LH release
is stimulated by gonadotropin-releasing hormone (GnRH) and inhibited by estrogen
in females and testosterone in males in this pathway.
What does the Luteinizing hormone do?
LH hormone has various functions, and they differ between women and men. In both
sexes, LH contributes to the maturation of primordial germ cells. In men, LH causes
the Leydig cells of the testes to produce testosterone. In women, the LH hormone
triggers the creation of steroid hormones from the ovaries. Additionally, it helps
regulate the menstrual cycle length and order in females by playing roles in ovulation
and implantation of an egg in the uterus.[2]
Figure 1:
Brief Introduction of LH hormone
Role of LH hormone in Female Reproductive
System:
LH supports theca cells in the ovaries that provide androgens and hormonal
precursors for estradiol production. At the time of menstruation, FSH
initiates follicular growth, specifically affecting granulosa cells.[3] LH receptors are
also expressed on the maturing follicle with the rise in estrogens, which causes it to
produce more estradiol. Eventually, 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 the estrogen-mediated negative
feedback of GnRH in the hypothalamus, which then stimulates the release of LH
hormone from the anterior pituitary.[4]
However, another theory of the LH peak is a positive feedback mechanism
from estradiol. The levels keep rising through the follicular phase, and when they
reach an unknown threshold, this results in the peak of the LH.[5] This effect is
opposite from the usual negative feedback mechanism presented at lower levels. In
other words, the mechanism(s) are not yet clear. The increase in LH production only
lasts for 24 to 48 hours. This “LH surge” triggers ovulation, thereby not only releasing
the egg from the follicle but also initiating the conversion of the residual follicle into
a corpus luteum that, in turn, produces progesterone to prepare
the endometrium for possible implantation.
LH hormone is necessary to maintain luteal function for the second two weeks of the
menstrual cycle. If pregnancy occurs, LH levels will decrease, and luteal function will
instead be maintained by the action of hCG (human chorionic gonadotropin), a
hormone very similar to LH but secreted from the new placenta. Gonadal steroids
(estrogens and androgens) generally have negative feedback effects on GnRH-1
release at the level of the hypothalamus and the gonadotropes, reducing their
sensitivity to GnRH. Estrogens’ positive feedback also occurs in the gonadal axis of
female mammals and is responsible for the midcycle surge of LH that stimulates
ovulation. Although estrogens inhibit kisspeptin (Kp) release from kiss1 neurons in
the ARC, estrogens stimulate Kp release from the Kp neurons in the AVPV.
As estrogens’ levels gradually increase, the positive effect predominates, leading to
the LH surge. GABA-secreting neurons that innervate GnRH-1 neurons also can
stimulate GnRH-1 release. These GABA neurons also possess ERs and may be
responsible for the GnRH-1 surge. Part of the inhibitory action of endorphins on
GnRH-1 release is through inhibition of these GABA neurons. Rupture of the ovarian
follicle at ovulation causes a drastic reduction in estrogen synthesis and a marked
increase in progesterone secretion by the corpus luteum in the ovary, reinstating
predominantly negative feedback on the hypothalamic secretion of GnRH-1.[6]
Figure 2:
Role of LH in female reproductive system
Role of LH in the Male Reproductive System:
For men, luteinizing hormone stimulates the production of testosterone from Leydig
cells in the testes. Testosterone, in turn, stimulates sperm production and helps
accentuate male characteristics like a deep voice or growth of facial hair. LH hormone
acts upon the Leydig cells of the testis and is regulated by gonadotropin-releasing
hormone (GnRH).[7] The Leydig cells produce testosterone under the control of LH,
which regulates the expression of the enzyme 17β-hydroxysteroid
dehydrogenase that is used to convert androstenedione, the hormone produced by
the testes, to testosterone. Two major hormones control the onset of puberty: FSH
initiates spermatogenesis, and LH signals the release of testosterone.
An androgen that exerts both endocrine activity and intratesticular activity
on spermatogenesis. LH hormone is released from the pituitary gland and is
controlled by pulses of gonadotropin-releasing hormone. When bloodstream
testosterone levels are low, the pituitary gland is stimulated to release LH.[8] As the
levels of testosterone increase, it will act on the pituitary through a negative
feedback loop and consequently inhibit the release of GnRH and LH.
Androgens (including testosterone and dihydrotestosterone) inhibit monoamine
oxidase (MAO) in the pineal gland, leading to increased melatonin and reduced LH
and FSH by a melatonin-induced increase of Gonadotropin-Inhibitory Hormone
(GnIH)[9] synthesis and secretion. Testosterone can also be aromatized
into estradiol (E2) to inhibit LH. E2 decreases pulse amplitude and responsiveness to
GnRH from the hypothalamus onto the pituitary.[10] Changes in LH and testosterone
blood levels and pulse secretions are induced by changes in sexual arousal in human
males.[11]
Figure 3: Role of LH in male reproductive system
LH Related Diseases:
1. Excess LH
LH and FSH levels may be in the reproductive range in children with precocious
puberty of pituitary or central origin instead of the low levels typical for their age.
During the reproductive years, relatively elevated LH is frequently seen in patients
with polycystic ovary syndrome; however, it would be unusual for them to have LH
levels outside the normal reproductive range. Persistently high LH levels indicate
situations where the normal restricting feedback from the gonad is absent, leading to
a pituitary production of LH and FSH. While this is typical in menopause, it is
abnormal in the reproductive years. There it may be a sign of:
• Premature menopause
• Gonadal dysgenesis
• Turner syndrome
• Klinefelter syndrome
• Castration
• Swyer syndrome
• Polycystic ovary syndrome
• Certain forms of congenital adrenal hyperplasia
• Testicular failure
• Pregnancy
2. Deficiency LH
Diminished secretion of LH hormone can result in failure of gonadal function
(hypogonadism). This condition is typically manifest in males as failure in the
production of normal numbers of sperm. In females, amenorrhea is commonly
observed. Conditions with very low LH secretions include:
• Pasqualini syndrome
• Kallmann syndrome
• Hypothalamic suppression
• Hypopituitarism
• Eating disorder
• Female athlete triad
• Hyperprolactinemia
• Hypogonadism
• Gonadal suppression therapy
• GnRH antagonist
• GnRH agonist
Conclusion:
In women, the hormone stimulates the ovaries to produce estradiol. Two weeks into
a woman’s cycle, a surge in luteinizing hormone causes the ovaries to release an egg
during ovulation. If fertilization occurs, the luteinizing hormone will stimulate the
corpus luteum, producing progesterone to sustain the pregnancy. In addition to
producing FSH and LH, the anterior portion of the pituitary gland also produces the
hormone prolactin (PRL) in females. Prolactin stimulates the production of milk by
the mammary glands following childbirth. In short, the LH hormone also plays a role
in the development of ova, induction of ovulation, and stimulation of estradiol and
progesterone production by the ovaries.
People with high levels of luteinizing hormone may experience infertility because the
hormone directly impacts the reproductive system. In women, luteinizing hormone
levels that are too high are often connected to polycystic ovary syndrome, creating
inappropriate testosterone levels. Some genetic conditions, like Turner
syndrome or Klinefelter syndrome, can cause high levels of the hormone. People with
these conditions are often unable to reproduce. Low levels of the luteinizing
hormone can also cause infertility because insufficient levels will limit the production
of sperm or the ovulation process. Too little luteinizing hormone stops ovulation in
women or creates a deficiency in gonadotrophin-releasing hormone (GnRH)
secretion in men.
References
1. Ilahi S, Ilahi TB. StatPearls [Internet]. StatPearls Publishing; Treasure Island (FL):
May 1, 2020. Anatomy, Adenohypophysis (Pars Anterior, Anterior Pituitary)
2. Kumar P, Sait SF. Luteinizing hormone and its dilemma in ovulation
induction. J Hum Reprod Sci. 2011 Jan;4(1):2-7.
3. Bowen R (13 May 2004). “Gonadotropins: Luteinizing and Follicle Stimulating
Hormones”. Colorado State University. Retrieved 12 March 2012.
4. Mahesh VB (January 2012). “Hirsutism, virilism, polycystic ovarian disease, and
the steroid-gonadotropin-feedback system: a career retrospective”. American
Journal of Physiology. Endocrinology and Metabolism. 302 (1): E4–
E18. doi:10.1152/ajpendo.00488.2011. PMC 3328092. PMID 22028409.
5. Guyton and Hall Textbook of Medical Physiology 2006 page 1021
6. Norris DO, Carr JA (2013). Vertebrate Endocrinology. Academic Press.
p. 126. ISBN 978-0-12-396465-6.
7. “Male Medical Fertility Treatment: HCG + LH + Recombinant FSH To Increase
Sperm Count Through Spermatogenisis”. Archived from the original on
February 19, 2015. Retrieved 6 April2015
8. Ubuka T, Son YL, Tobari Y, Narihiro M, Bentley GE, Kriegsfeld LJ, Tsutsui K
(2014). “Central and direct regulation of testicular activity by gonadotropin-
inhibitory hormone and its receptor”. Frontiers in Endocrinology.
9. Pitteloud N, Dwyer AA, DeCruz S, Lee H, Boepple PA, Crowley WF, Hayes FJ
(March 2008). “Inhibition of luteinizing hormone secretion by testosterone in
men requires aromatization for its pituitary but not its hypothalamic effects:
evidence from the tandem study of normal and gonadotropin-releasing
hormone-deficient men”. The Journal of Clinical Endocrinology and
Metabolism. 93(3): 784–91. doi:10.1210/jc.2007-
2156. PMC 2266963. PMID 18073301.
10. Stoléru SG, Ennaji A, Cournot A, Spira A (1993). “LH pulsatile secretion and
testosterone blood levels are influenced by sexual arousal in human
males”. Psychoneuroendocrinology. 18 (3): 205–18. doi:10.1016/0306-
4530(93)90005-6. PMID 8516424.
11. Weiss J, Axelrod L, Whitcomb RW, Harris PE, Crowley WF, Jameson JL (January
1992). “Hypogonadism caused by a single amino acid substitution in the beta
subunit of luteinizing hormone”. The New England Journal of
Medicine. 326 (3): 179–83.
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