The document provides information on sex hormones including:
1. It discusses the history of discoveries related to female reproductive hormones including the establishment of ovarian control and isolation of estrogen.
2. It describes the types of estrogens including natural estrogens like estradiol and synthetic estrogens used orally.
3. It explains progesterone's role in the menstrual cycle and pregnancy, how it is synthesized and secreted, and its physiological actions in various body systems.
The two main sex hormones — estrogen and testosterone — have wide-ranging effects in the body. Produced primarily by the ovaries (estrogen) and testes (testosterone), these hormones affect not just your sexual function but also your bones, brain, and blood vessels.
The two main sex hormones — estrogen and testosterone — have wide-ranging effects in the body. Produced primarily by the ovaries (estrogen) and testes (testosterone), these hormones affect not just your sexual function but also your bones, brain, and blood vessels.
What is sex hormone ?
Sex hormones are synthesized from cholesterol and secreted throughout a person's lifetime
at different levels.
Male gonads (testes) produce sperm.
Female gonads (ovaries) produce egg.
Fusion of egg and sperm occur via fertilization to produce a zygote.
The zygote undergoes division to become an embryo, which eventually becomes a fetus.
What is sex hormone ?
Sex hormones are synthesized from cholesterol and secreted throughout a person's lifetime
at different levels.
Male gonads (testes) produce sperm.
Female gonads (ovaries) produce egg.
Fusion of egg and sperm occur via fertilization to produce a zygote.
The zygote undergoes division to become an embryo, which eventually becomes a fetus.
Đối với phụ nữ, nội tiết tố nữ được ví như nhựa sống cho cơ thể. Khi tình trạng mất cân bằng nội tiết tố xuất hiện có thể gây ra những ảnh hưởng lớn đối với cơ thể. Để hiểu rõ về nội tiết tố là gì, tác dụng ra sao, nguyên nhân gây mất cân bằng cách điều trị hiệu quả hãy cùng tham khảo bài viết sau.
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Hormonal Control of Reproductive Process in FemalesPRANJAL SHARMA
The hormones controlling the female reproductive system include gonadotropin-releasing hormone (GnRH), follicle-stimulating hormone (FSH) and leutenizing hormone (LH), all of which are produced in the brain; oestrogen and progesterone produced by the ovaries and the corpus luteum; and human chorionic gonadotropin (HCG).
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2. HISTORY:-
Hormones in the Female Reproductive System
❖ The hormonal nature of the ovarian control of the female reproductive system
was firmly established in 1900 by Knauer when he found that ovarian
transplants prevented the symptoms of gonadectomy, and by Halban, who
showed that normal sexual development and function occurred when glands
were transplanted.
❖ In 1923, Allen and Doisy devised a bioassay for ovarian extracts based on the
vaginal smear of the rat. Frank and associates in 1925 detected an active sex
principle in the blood of sows in estrus, and Loewe and Lange discovered in
1926 that a female sex hormone varied in the urine of women throughout the
menstrual cycle.
❖ The excretion of estrogen in the urine during pregnancy also was reported by
Zondek in 1928 and enabled Butenandt and Doisy in 1929 to crystallize an active
substance.
❖ The active principle estradiol was obtained in pure form in 1929 and soon its
chemical structure was worked out.
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3. TYPES OF ESTROGEN:
❖Natural estrogens :
➢ Estradiol is the major estrogen secreted by the ovary. It is synthesized in the
graafian follicle, corpus luteum and placenta from cholesterol.
➢ Estradiol is rapidly oxidized in liver to estrone which is hydroxylated to form
estriol.
➢ All three are active and circulate in blood, but estradiol is the most potent
estrogen.
❖Synthetic estrogens
➢ Natural estrogens are inactive orally and have a short duration of action due to
rapid metabolism in liver. To overcome this, synthetic compounds have been
produced
▪ Steroidal : Ethinylestradiol, Mestranol, Tibolone.
▪ Nonsteroidal : Diethylstilbestrol (stilbestrol) Hexestrol, Dienestrol
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4. ➢ Steroidal estrogens arise from androstenedione or
testosterone by aromatization of the A ring. The reaction is
catalyzed by aromatase (CYP19) that uses nicotinamide
adenine dinucleotide phosphate (NADPH) and molecular
oxygen as co-substrates.
➢ A ubiquitous flavoprotein, NADPH -cytochrome P450 reductase,
also is essential. Both proteins are localized in the endoplasmic
reticulum of ovarian granulosa cells, testicular Sertoli and
Leydig cells, adipose stroma, placental syncytiotrophoblasts.
preim-plantation blastocysts, bone, various brain regions, and
many other tissues.
➢ The ovaries are the principal source of circulating estrogen in
premenopausal women, with estradiol the main secretory
product.
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5. ➢ Gonadotropins, acting via receptors that couple to the G-
adenylylcyclase cyclic AMP pathway, increase the activities of
aromatase and the cholesterol side- chain cleavage enzyme and
facilitate the transport of cholesterol (the precursor of all
steroids) into the mitochondria of cells that synthesize steroids.
➢ The ovary contains a form of 17β-hydroxy steroid dehydrogenase
(type 1) that favors the production of testosterone and estradiol
from androstenedione and estrone.
➢ However, in the liver, another form of this enzyme (typeЦ ) favors
oxidation of circulating estradiol to estrone. and both of these
steroids are then converted to estriol .
➢ All three of these estrogens are excreted in the urine along with
their glucuronide and sulfate conjugates.
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9. ❖The menstrual cycle.
➢The menstrual cycle is divided into the follicular phase and the luteal
phase. Ovulation defines the transition between these two phases.
➢ During the follicular phase, gonadotroph cells of the anterior pituitary gland
secrete LH and FSH in response to pulsatile GnRH stimulation. Circulating LH
and FSH promote growth and maturation of ovarian follicles.
➢ Developing follicles secrete increasing amounts of estrogen. At first, the
estrogen has an inhibitory effect on gonadotropin release. Just before the
midpoint in the menstrual cycle, however, estrogen exerts a brief positive
feedback effect on LH and FSH release.
➢ This is followed by follicular rupture and release of an egg in to the fallopian
tube. During the second half of the cycle, the corpus luteum secretes both
estrogen and progesterone. Progesterone induces a change in the endometrium
from a proliferative to a secretory type.
➢ If fertilization and implantation of a blastocyst do not occur within 14 days after
ovulation, the corpus luteum involutes, secretion of estrogen and progesterone
declines, menses occurs, and a new cycle begins.
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10. ❖Estrogen Receptors
➢ Estrogens exert their effects by interaction with receptors that are
members of the superfamily of nuclear receptors
➢ The two ER genes are located on separate chromosomes: ESR1
encodes ERα, and ESR2 encodes ERβ.
➢ ERα is expressed most abundantly in the female reproductive
tract—especially the uterus, vagina, and ovaries—as well as in
the mammary gland, the hypothalamus, endothelial cells, and
vascular smooth muscle.
➢ ERβ is expressed most highly in the prostate and ovaries, with
lower expression in lung, brain, bone, and vasculature.
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11. ❖Mechanism ofAction
➢ Both ERs are ligand-activated transcription factors that increase
or decrease the transcription of target genes . After entering the
cell by passive diffusion through the plasma membrane, the
hormone binds to an ER in the nucleus. In the nucleus, the ER is
present as an inactive monomer bound to HSP90, and on binding
estrogen, a change in ER conformation dissociates the HSPs and
causes receptor dimerization, which increases the affinity and the
rate of receptor binding to DNA .
➢ The ER dimer binds to EREs, typically located in the promoter
region of target genes. The ER/DNA complex recruits a cascade
of co-activator and other proteins to the promoter region of
target genes and allows the proteins that make up the general
transcription apparatus to assemble and initiate transcription.
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13. ❖ Physiological and PharmacologicalActions
❖Developmental Actions:
✓ Estrogens are largely responsible for pubertal changes in girls
and secondary sexual characteristics. They cause growth and
development of the vagina, uterus, and fallopian tubes, and
contribute to breast enlargement.
✓ They also contribute to molding the body contours, shaping the
skeleton, and causing the pubertal growth spurt of the long
bones and epiphyseal closure. Growth of axillary and pubic hair,
pigmentation of the genital region, and the regional
pigmentation of the nipples and areolae that occur after the
first trimester of pregnancy are also estrogenic actions.
Androgens may also play a secondary role in female sexual
development.
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14. ✓ In male, estrogen deficiency diminishes the pubertal growth
spurt and delays skeletal maturation and epiphyseal closure so
that linear growth Continues into adulthood.
✓ Estrogen deficiency in men leads to elevated gonadotropins.
macroorchidısm, and increased testosterone levels and also may
affect carbohydrate and lipid metabolism and fertility in some
individuals.
✓ Controlling menstrual cycle in female .
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15. Antiestrogen and SERMs
➢Selective Estrogen Receptor Modulators (SERMs).
➢Are mixed agonists/antagonists.
➢Tamoxifen -an ER antagonist in breast, but a partial
agonist in
➢endometrium and bone.
➢Raloxifene - ER agonist in bone, but an antagonist in
both breast and endometrium.
➢Clomifene - used to induce ovulation. Is an ER antagonist
in
➢Hypothalamus and ant pit, but a partial agonist in
ovaries.
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17. ➢Progesterone is also a steroid. Anatural hormone secreted by
the corpus luteum and the placenta.
➢Intestinal absorption is quite erratic; must be micronized for most
➢effective absoption.
➢Important in menstrual cycle and pregnancy.
➢Used for hormonal contraception and for producing long-term
ovarian suppression for other purposes (e.g.,dysmenorrhea,
endometriosis, hirsutism and bleeding disorders) when estrogens are
contra-indicated.
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18. ❖Biosynthesis and Secretion
➢ Progesterone is secreted by the ovary, mainly from the corpus
luteum, during the second half of the menstrual cycle.
➢ LH, acting via its G protein–coupled receptor, stimulates
progesterone secretion during the normal cycle.
➢ After fertilization, the trophoblast secretes hCG into the maternal
circulation, which then stimulates the LH receptor to sustain the
corpus luteum and maintain progesterone production.
➢ During the second or third month of pregnancy, the developing
placenta begins to secrete estrogen and progesterone in
collaboration with the fetal adrenal glands, and thereafter the
corpus luteum is not essential to continued gestation
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19. ❖Physiologic Actions
❖Neuroendocrine Actions :
➢Progesterone produced in the luteal phase of the cycle has
several physiological effects, including decreasing the frequency of
GnRH pulses. This progesterone-mediated decrease in GnRH
pulse frequency is critical for suppressing gonadotropin release
and resetting the hypothalamic pituitary-gonadal axis to transition
from the luteal back to the follicular phase.
❖Reproductive Tract:
➢Progesterone decreases estrogen-driven endometrial
proliferation and leads to the development of a secretory
endometrium , and the abrupt decline in progesterone at the end
of the cycle is the main determinant of the onset of menstruation.
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20. ❖Mammary Gland :
➢Development of the mammary gland requires both estrogen and
progesterone. During pregnancy and to a minor degree during the
luteal phase of the cycle, progesterone, acting with estrogen, brings
about a proliferation of the acini of the mammary gland. Toward the
end of pregnancy, the acini fill with secretions, and the vasculature of
the gland notably increases; however, only after the levels of estrogen
and progesterone decrease at parturition does lactation begin.
❖Metabolic Effects:
➢Progestins have numerous metabolic actions. Progesterone
itself increases basal insulin levels and the rise in insulin after
carbohydrate ingestion, but it does not normally alter glucose
tolerance. However, long-term administration of more potent
progestins, such as norgestrel, may decrease glucose tolerance.
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21. ❖Mechanism ofAction
➢ Asingle gene encodes two isoforms of the PR, PR-A and PR-B. The first 164 N-
terminal amino acids of PR-B are missing from PR-A; this occurs by use of two
distinct estrogen-dependent promoters in the PR gene.
➢ PR is present primarily in the nucleus in an inactive monomeric state bound to
HSP90, HSP70, and p59. When receptors bind progesterone, the HSPs
dissociate, and the receptors are phosphorylated and subsequently form dimers
(homo- and heterodimers) that bind with high selectivity to PREs located on
target genes . Transcriptional activation by PR occurs primarily via recruitment
of co-activators such as SRC1, NcoA-1, or NcoA-2 .
➢ The receptor-coactivator complex then favors further interactions with
additional proteins, such as CBP and p300, which mediate other processes,
including histoneacetylase activity.
➢ Histone acetylation causes remodeling of chromatin that increases the
accessibility of general transcriptional proteins, including RNA polymerase II, to
the targetpromoter.
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22. Antiprogestin
❖Mifepristone:
➢It is 19-norsteroid with potent competitive
antiprogesterone.
➢Given during the follicular phase
➢Slowing of follicular development / failure of
ovulation.
➢During luteal phase
➢Prevent progesterone secretion.
➢Orally active
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24. ❖ANDROGENS :
(Male Sex Hormones)
➢ Androgens are substances which cause development of
secondary sex characters in the castrated male. That testes
are responsible for the male characters is known since
prehistoric times.
➢ Its endocrine function was established by Berthold in 1849.
Testosterone was isolated as the testicular hormone, its
structure was worked out and it was synthetically prepared
by theyear 1935.
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25. ❖Types of androgens :
❖Natural androgens :
❖ Testes of adult male produce 5–12 mg of testosterone daily, a part
of which is converted in extraglandular tissues to the more active
dihydrotestosterone (DHT); by the enzyme steroid 5 α-reductase.
❖ Adrenal cortex produces small quantities of
dehydroepiandrosterone and androstenedione which are called
‘weak androgens’ (potency 1/20 to 1/30).
❖Synthetic androgens :
❖ Methyltestosterone and fluoxymesterone are 17-alkyl substituted
derivatives of testosterone which are orally active because of
resistance to first pass metabolism.
❖ANABOLIC STEROIDS
❖ These are synthetic androgens with supposedly higher anabolic
and lower androgenic activity. Drugs are Nandrolone,
Oxymetholone, Stanozolol and Methandienone. 25
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26. ➢Regulation of secretion
➢ Testosterone is secreted by the interstitial (Leydig) cells of the
testes under the influence of pulsatile secretion of LH from
pituitary.
➢ FSH is mainly responsible for promotion of spermatogenesis in
tubular (Sertoli) cells.
➢ The mediator of feedback relationship with pituitary is uncertain.
While relatively high concentration of testosterone inhibits LH
secretion and in time causes atrophy of interstitial cells.
➢ It has only weak inhibitory action on FSH secretion. Estrogens
are more potent inhibitors of Gn secretion even in males, and it is
believed that the small amount of estradiol produced by testes as
well as that resulting from conversion of testosterone to estradiol
in liver and fat plays a role in feedback inhibition.
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27. ▪ In liver and many target cells 5α-reductase enzyme
converts testosterone to the more potent androgen
dihydrotestosterone (DHT) which combines more
avidly with the androgen receptor (AR).
▪ The aromatase enzyme in testes, liver and adipose
tissue converts some testosterone into estradiol
which exerts certain actions in male target cells by
combining with estrogen receptor (ER) and is
probably important for feedback inhibition of
gonadotropins (LH/FSH) as well as that of
gonadotropin releasing hormone (GnRH) from
hypothalamus.
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30. ❖ACTIONS :
❖Sex organs and secondary sex characters
1. Growth of genitals—penis, scrotum, seminal
vesicles, prostate.
2. Growth of hair—pubic, axillary, beard, moustache,
body hair and male pattern of its distribution.
Thickening of skin which becomes greasy due to
proliferation and increased activity of sebaceous
glands—especially on the face. The duct often gets
blocked and infection occurs resulting in acne.
Subcutaneous fat is lost and veins look prominent.
❖Testes :
• Testosterone is needed for normal spermatogenesis
and maturation of spermatozoa. 30
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31. ❖Skeleton and skeletal muscles (Anabolic)
➢ Rapid bone growth, both in thickness as well as in
length After puberty, the epiphyses fuse and linear
growth.
➢ Estradiol largely mediates the effect of testosterone on
bone mineralization.
➢ Testosterone also promotes muscle building, especially if
aided by exercise.
❖Erythropoiesis
➢ Testosterone accelerates erythropoiesis by increasing
erythropoietin production and probably direct action on
haeme synthesis. Men have higher hematocrit than
women.
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32. ❖PHARMACOKINETICS
➢ Testosterone is inactive orally due to high first pass metabolism in
liver. The duration of action after i.m. injection is also very short.
➢ Therefore, slowly absorbed esters of testosterone are used by this
route—are hydrolysed to the active free form. Testosterone in
circulation is 98% bound to sex hormone binding globulin
(SHBG) and to albumin.
➢ The SHBG bound testosterone is unavailable for action due to
tight binding. The major metabolic products of testosterone are
androsterone and etiocholanolone which are excreted in urine,
mostly as conjugates with glucuronic acid and sulfate.
➢ Small quantities of estradiol are also produced from testosterone
by aromatization of A ring in extraglandular tissues (liver, fat,
hypothalamus). Plasma t½ of testosterone is 10–20 min.
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33. ❖DNA Dependent Actions of the AR
➢ The DNA binding-dependent actions of the AR are also commonly
➢referred to as ‘genomic’, ‘classical’or‘canonical’AR signalling.
➢ In the absence of ligand, the AR is cytoplasmic, associated with
heat-shock and other chaperone proteins. Androgens bind to the
AR, resulting in a conformational change, dissociation of
chaperone proteins and exposure of the NLS.
➢ The androgen/AR complex translocates to the nucleus where it
dimerises and binds to AREs within classical target genes to
modulate genetranscription.
➢ The transcriptional activity of the androgen-bound AR is
modulated by specific proteins known as coregulators.
Coregulators bind to the activated AR in a ligand-dependent
manner to either enhance (co-activator) or repress (corepressor)
its ability to transactivate the target gene through chromatin
remodelling and histonemodification. 33
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35. ❖Side effects
➢ Anabolic steroids were developed with the idea of
avoiding the virilizing side effects of androgens while
retaining the anabolic effects.
➢ But the same adverse effect profile applies to these
compounds. The 17-alkyl substituted compounds
oxymetholone, stanozolol, can produce jaundice and
worsen lipid profile.
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36. ❖Uses :
✓ Testicular failure It may be primary—in children, resulting in
delayed puberty. Treatment with parenteral testosterone esters
or transdermal testosterone/dihydrotestosterone in courses of
4–6 months at a time is highly satisfactory.
✓ Hypopituitarism Hypogonadism is one of the features of
hypopituitarism. Androgens are added at the time of puberty to
other hormonal replacement.
✓ . AIDS related muscle wasting Testosterone therapy has
been shown to improve weakness and muscle wasting in
AIDS patients with low testosterone levels.
✓ Ageing Because testosterone levels decline in old age, it has
been administered to elderly males to improve bone
mineralization and musclemass.
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37. ✓ Osteoporosis: In elderly males and that occurring due to
prolonged immobilization may respond to anabolic steroids,
but bisphosphonates are more effective and are the preferred
drugs.
✓ To enhance physical ability in athletes When administered
during the period of training androgens/anabolic steroids
can increase the strength of exercised muscles. However,
effects are mostly short-lived and the magnitude of
improvement in performance is uncertain except in women.
This is considered illegal and anabolic steroids are included
in the list of ‘dope test’ performed on athletes before
competitive games.
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38. ❖Referance :
➢ G & G 13 th edition ,Androgens and the Male
Reproductive Tract by (Peter J. Snyder) . Chapter no.
45 , page no: 833
➢ Essentials of Medical Pharmacology, by K.D. Tripathi
7th edition. Chapter 21, page no: 298.
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