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Sex steroids Flashcards

1
Q

What are hormones?

A
  • chemical messengers secreted by the endocrine glands
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2
Q

What is the function of hormones?

A
  • Communicate regulatory messages within the body
  • Control metabolism , behaviour necessary for organisms to survive and produce?
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3
Q

What are autocrine hormones?

A

Hormones that communicate within cells

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4
Q

What are paracrine hormones?

A

Hormones that act directly upon a nearby cell

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5
Q

What are juxtracrine hormones?

A

Hormones that work between connecting cells, requires physical contact of two cells.

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5
Q

What are endocrine hormones?

A

Hormones that are transported in the blood to a distant site of action

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6
Q

What are examples of steroidal hormones?-

A
  • Adrenal cortical hormones (corticoids)
  • Sex hormones
  • Peptide hormones
  • Amino acid derivative
  • Miscellaneous
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7
Q

What are the female sex hormones?

A

Oestrogen and progesterone

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7
Q

What are the male sex hormones?

A

Androgens

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8
Q

What is the role of steroid hormones?

A
  • Regulate diverse physiological functions e.g. reproduction, blood salt balance, maintenance of secondary sexual characteristics, response to stress, neuronal function and various metabolic processes (fat. muscle, bone mass).
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9
Q

What is progesterone?

A
  • A steroid hormone released by the corpus luteum (luteal phase of mc) that stimulates the uterus to prepare for pregnancy
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10
Q

What are steroids?

A
  • Lipophilic, low-molecular weight compounds

– Cholesterol derived

  • synthesised in the :

– adrenal cortex

– Ovaries

– Testes

– Ovarian corpus luteum

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11
Q

How are steroids biosynthesised?

A

-Requires several distinct Cytochrome P450 enzymes

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12
Q

What is Oestrone?

A

-Weaker than Oestradiol

-produced in fat tissue from precursors made from adrenal glands

-important after Menopause

-Main oestrogen in men

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13
Q

What is steroidogenesis?

A
  • Production of steroid hormones
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14
Q

What is the first step in steroidogenesis?

A
  • The enzymatic modification of cholesterol
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15
Q

What are sources of cholesterol?

A
  • production of steroid hormones
    1.) Dietary

2.) De novo biosynthesis. Starts from co-enzyme A in the cytosol

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16
Q

What does steroidogenic acute regulatory protein do?

A
  • STAR protein - facilitates the movement of cholesterol from the cytoplasm to mitochondria
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17
Q

What are androgens?

A

-Steroid hormones that control the expression and maintenance of male sexual characteristics.

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18
Q

What are adrenal androgens?

A

Sex hormones that supplement those made in gonads (DHE.A and Androstenedione)

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19
Q

What are the different zones of the adrenal cortex?

A
  • Zona glomerulosa
  • Zona fasciculata
  • Zona reticularis
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20
Q

What zone of the adrenal cortex secretes aldosterone?

A

Zona glomerulosa

21
Q

What zone of the adrenal cortex secretes cortisol?

A

Zona fasciculata

22
Q

What zone of the adrenal cortex secretes androgens?

A

Zona reticularis

23
Q

Where is testosterone secreted?

A
  • In the testes by Leydig cells ( lie between the seminiferous tubules
  • stimulated by luteinizing hormone
24
Q

How are Leydig cell populations divided?

A
  • into foetal Leydig cells that operate prenatally, and the adult-type Leydig cells that are active postnatal
  • Foetal LC are the primary source of testosterone
  • rely heavily on de novo cholesterol synthesis
25
Q

How is testosterone biosynthesis regulated?

A

-under the control of LH which regulates the expression of 17 beta hydroxisteroid dehydrogenase.
- When testosterone levels are low GnRH is released from the hypothalamus which in turn stimulates the pituitary gland to release FSH and LH. These later stimulate the testis to synthesise testosterone.
- Increasing the levels of a testosterone through a negative feedback loop act on the hypothalamus and pituitary gland to inhibit the release of GnRH and FSH/LH

26
Q

How are sex hormones transported?

A
  • Hydrophobic/Lipophilic
  • Not easily dissolvable in blood
  • Carrier needed ( only a small amount is free 2%)
  • Non specific and specific carrier proteins
27
Q

What are examples of non specific carrier proteins?

A
  • Non specific carrier proteins ( such as ALBUMIN - most abundant plasma protein. Transports almost any lipophilic molecule that enters the bloodstream)
28
Q

What are examples of specific carrier proteins?

A
  • Corticosteroid Binding Globulin (CBG) specific for Glucocorticoids
  • Thyroid binding globulin (TBG) - specific for Thyroid hormones
  • Sex hormone binding globulin (SHBG) - specific for oestradiol and testosterone
29
Q

What influences bioavailability of sex hormones?

A
  • the level of SHBG (Sex hormone binding globulin)
  • lower in men than women
  • levels of shbg in men start to low during puberty and stabilise during puberty
  • Endogneous /exogenous thyroid hormones / oestrogens increase SHBG levels
30
Q

What is the SHBG relative binding affinity?

A
  • SHBG binds sex steroids with high affinity (KD approx., 10 [-10] M)
  • DHT> TESTOSTERONE> ANDROSTENEDIOL> OESTRADIOL> OESTRONE
  • Higher affinity for DHT and testosterone compared to oestrogen
  • Increased SHBG levels may be associated with hypogonadism in men and decreased levels can result in androgenisation in women.
  • Can affect the balance between bioavailable androgens/ estrogens
31
Q

What two main mechanisms do the effects of testosterone occur by?

A
  • Activation of androgen receptor AR (directly or as DHT)
  • Conversion to oestradiol and activation of oestrogen receptors
32
Q

How does testosterone work in target cells?

A
  • acts intracellularly
  • Androgen receptors - AR nuclear receptor membranes of transcription factors superfamily
  • composed of a single polypeptide chain that has 3 distinct domains:
  • N-terminal domain : highly variable sequence involved in activating or stimulating transcription
  • DNA binding domain DBD : Region responsible for binding of the receptor to specific sequences of DNA
  • conservative region
    -specificity is given by binding region of gene having an Androgen response element
  • Ligand-binding domain : hormone binding region
33
Q

What are the mechanisms of ligand-dependent androgen receptor action?

A

1.) DBD signalling
- Androgens bind to AR, resulting in a conformational change. Dissociation of chaperone proteins and the AR complex translocate to the nucleus where it dimerises and binds to AREs within classical target genes to modulate gene transcription
2.) Non-DBD signalling
- The AR complex can signal through Non DBD pathways. Activation of 2nd messenger pathways (AP-1,ERK,Akt and MAPK kinase.)

34
Q

What are the effects of testosterone at different stages of life?

A
  • Foetal : Male internal genitalia (epididymis, vas deferens and seminal vesicles) and male external genitalia (penis, scrotum, prostate)
  • Puberty- increase in testosterone production and mature sperm production. Increased secretion of testosterone into the systemic circulation affects many tissues simultaneously.
  • Adulthood - gradual development of male pattern baldness, gradual development of benign prostatic hyperplasia
  • Senescence : serum testosterone concentration gradually declines contributing to decreases in energy , libido, muscle mass , and strength, and bone mineral density.
35
Q

What are some therapeutic uses of androgens?

A
  • Male Hypogonadism (testosterone deficiency)
  • Female hypogonadism
  • Hypopituitarism
    -AIDS related muscle wasting
  • Male senescence
  • Hereditary angioneurotic oedema
36
Q

What are some biologically important oestrogens and progestins?

A
  • Oestradiol 17 beta - most potent oestrogen naturally found in women
  • Progesterone: - the most important naturally occurring progestin
37
Q

What are the main function of the ovaries?

A
  • To produce oocytes in prep for fertilisation
  • To produce oestrogen and progesterone in response to LH and FSH
  • A principal source of circulating oestrogen in premenopausal women (oestradiol = main secretory product)
38
Q

What is the basic reproductive/endocrine unit of the ovary?

A
  • A single ovarian follicle
  • composed of one germ cell that is surrounded by a cluster of endocrine cells, organised in two layers separated by a basal membrane
  • inner layer surrounding the oocyte is composed of granulosa cells and the outer layer is composed of theca cells
39
Q

What is the steroidogenesis of the ovaries?

A
  • cholesterol is derived from the uptake of plasma LDL
  • Pregnenolone is converted inro progesterone in the corpus luteum
  • In theca cells, pregnenolone is converted to androstenedione precursor of oestrogens produced in the granulosa cells
  • Oestradiol in the liver is oxidated by 17 Beta- hydroxysteroid dehydrogenase type II to estrone and then to estriol
40
Q

How are oestrogen and progestin production regulated?

A
  • In theca cells, LH controls 17BHSD activity and androstenedione production, whereas CYP19 (P450arom) activity in the granulosa cells is controlled by FSH and oestradiol production
  • LH acts on both thecal and granulosa cells; FSH acts only on granulosa cells. FSH and
    LH stimulate adenylate cyclase via G protein-coupled receptors. Cyclic adenosine
    monophosphate (cAMP) generated from adenosine triphosphate (ATP) activates protein
    kinase A, which in turn stimulates steroidogenic enzymes.
41
Q

What are the physiological actions of Oestrogens?

A
  • largely responsible for pubertal changes in girls and secondary sexual characteristics
  • essential for the development and maintenance of the female phenotype, germ cell maturation and pregnancy

Sex organs:
— Growth of uterus, fallopian tubes and vagina
— Menstruation in anovulatory cycles
— Enhances sperm penetration
— Deficiency leads to atrophic changes in female reproductive tract
Secondary Sex Characters: — Breasts: proliferation of ducts and stroma, accumulation of fat
— Pubic and axillary hair appears
— Feminine body contours and behaviours
* In boys, oestrogen deficiency diminishes the pubertal growth spurt and delays skeletal
maturation and epiphyseal closure so that linear growth continues into adulthood.

42
Q

How do oestrogens control the menstrual cycle?

A

Oestrogen, during mid puberty, exerts a
positive feedback on gonadotropin-releasing
hormone (GnRH) secretion.
Leads to the progressive increase of LH and
FSH production, culminating in the LH surge,
ovulation, and the initiation of the menstrual
cycle.
In the adult female, oestrogen plays a critical
role in maintaining the menstrual cycle.

43
Q

What are the metabolic effects of Oestrogen?

A
  • Anabolic Responsible for pubertal growth spurt in both boys and girls
  • Bone Mass Retards bone resorption; Promotes fusion of epiphyses.
  • Lipid metabolism Increase of high-density lipoprotein (HDL) levels and decrease of levels of
    low-density
  • lipoprotein (LDL) and lipoproteinA (LPA).
  • Blood coaugulability Increase in coagulation factors Il, Vll, IX, X, and Xll, and increase fibrinolitic activity ( decreased levels of plasminogen-activator inhibitor 1 PAI-I ).
  • Vasvular endothelium Promote vasodilation and retard atherogenesis (increase of NO
    levels).
  • Gallbladder Alter bile composition by increasing cholesterol secretion and decreasing bile
    acid secretion.
  • Glucose Impaired glucose tolerance due to increased insulin resistance
44
Q

What are oestrogen receptors?

A
  • Estrogen Receptor Alpha (ERa) and Beta (ERB)
  • subtyped expressed by most tissues
    ERA:
  • predominates in uterus, vagina, breast, bone, hypothalamus, blood vessels
    ERB:
  • predominates in : Prostate gland of males, ovaries in females
  • E2 bind to both receptors with equal affinity
  • receptors have different pattern of interaction (different activity) with coactivators and corepressirs
45
Q

What is the genomic mechanism of action of oestrogen?

A
  • Genomic mechanism:
  • enters the vell by passive diffusion through the plasma membrane and binds to an ER in the nucleus
  • In the nucleus, the ER is present as an inactive monomer bound to a heat-shock protein 90 which dissociates after hormones binding with subsequent receptor dimerization
  • The ER dimer binds to oestrogen response elements (EREs), typically located in the promoter region of target genes

Non genomic mechanisms:
- Interaction of hormones with oestrogen receptors located on the plasma membrane of cells
- These membrane localised ERs mediate the rapid activation of some proteins such as MAPJ and the rapid increase in CAMPS caused by the hormone.

46
Q

Therapeutic uses of Oestrogen

A
  • Hormonal Replacement Therapy
  • Senile Vaginitis
  • Delayed puberty in girls
  • Dysmenorrhea
  • Dysfunctional uterine bleeding
  • Carcinoma prostate
47
Q

How are progestins synthesised and metabolised?

A
  • Progesterone is secreted by the ovary, mainly from the corpus luteum, during the second half of the menstrual cycle from the placenta during the 2nd/3rd month of pregnancy
  • Progesterone is rapidly metabolised by the liver. It is converted to pregnanediol and conjugated to glucuronic acid in the liver. Pregnanediol glucuronide is excreted in the urine.
48
Q

What are the Physiological actions of progesterone in the reproductive tract?

A
  • Decreases oestrogen-driven endometrial proliferation and leads to the development of a secretory endometrium
  • Important in the maintenance of pregnancy and suppression of menstruation and uterine contractility
  • Increases the viscosity of cervical mucus
49
Q

What are the physiological actions of progesterone in the mammary gland?

A
  • Proliferation of the acini of the m gland during pregnancy and cyclic epithelial proliferation and turnover of acini during luteal phase
  • Control of mitotic activity in the breast epithelium
  • Preparation of breast for lactation
50
Q

What are the physiological actions of progesterone in the CNS?

A
  • Depressant and hypnotic actions
  • Increase in basal body temperature
  • Increase of the ventilatory response to CO2 and reduction of arterial and alveolar PCO2

Metabolic effects
- increases basal insulin levels
- Stimulation of lipoprotein lipase activity and enhancement of fat deposition

51
Q

What is the mechanism of action of progesterone?

A

Two isoforms PR-A and PR-B.
* In the absence of ligand, PR is present in the nucleus in
an inactive monomeric state bound to heat-shock proteins
* (HSP-90, HSP-70, and p59).
* When receptors bind progesterone, the heat-shock
proteins dissociate, and the receptors are phosphorylated
and subsequently form dimers (homo- and heterodimers)
that bind with high
* selectivity to PREs (progesterone response elements)
located on target genes.
In most cells, PR-B mediates the stimulatory activities of
progesterone; PR-A strongly inhibits this action of PR-B
and is also a transcriptional inhibitor of other steroid
receptors.
o: rapid effects as well as Ca++ release from spermatozoa
and Oocyte maturation.

52
Q

What are therapeutic uses of progesterone?

A
  • Contraception
  • HRT for non-hysterectomised postmenopausal women to counteract risk of endometrial carcinoma
  • Dysfunctional uterine bleeding
  • Endometriosis
  • PMS/tension
  • Threatened/ habitual abortion
  • Endometrial carcinoma

Reproduction (22 decks)

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