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Endocrine & Diabetes > Gonadal Steroidogenesis and Actions > Flashcards

Gonadal Steroidogenesis and Actions Flashcards

1
Q

What are the actions of mineralocorticoids and where are they made?

A

-salt & water retention
(Na+ & K+ electrolyte
& fluid balance)
=Ring structure protecting 11 beta position
=C21
-Zone-specific expression of aldosterone synthase determines aldosterone production in the adrenal zona glomerulosa

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2
Q

What are the actions of glucocorticoids and where are they made?

A

-glucose synthesis, protein metabolism, inflammation, immune response
=11 hydroxyl group (cortisol, if cleaved off= cortisone)
=C21
-Zone-specific expression of 17α-OHase & 11ß-OHase determines cortisol production in the adrenal zona fasciculata

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3
Q

What are the actions of adrenal androgens and where are they made?

A

-foetal development, foetal oestrogenic environment, postmenopausal oestrogens
=C19
=Carbon groups clipped off
-Zone-specific expression of 17α-OHase & 17, 20 lyase determines DHEA production in the adrenal zona reticularis

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4
Q

What is the link between cortisone and reproductive tissues?

A

-Cortisone is activated to cortisol in reproductive tissues

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5
Q

What are the key human sex steroids synthesised in reproductive tissues?

A

-Progesterone= menstrual cycle maintenance of pregnancy
=C21 progestogen female steroid
-Androgens= growth and function of male reproductive system
=Testosterone C19 androgen male steroid
-Oestrogens= growth and function of female reproductive system
=oestradiol C18 oestrogen female steroid

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6
Q

What are the types of enzymes involved in human sex steroid hormone synthesis?

A
  • Cytochrome P450s (CYPs)

- Steroid dehydrogenases

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7
Q

Describe CYPs

A

=cleave cholesterol side chains
-17-OHase/17, 20 lyase (CYP17A1)
=adrenal cortex ZR
=testis, ovary

-Aromatase (CYP19A1)
= ovary (male testosterone to oestradiol)
= AND peripheral oestrogen targets
=e.g. breast, bone, etc.
= (aromatase inhibitors used to treat cancer)

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8
Q

Describe Steroid dehydrogenases

A

-interconvert steroids
=3β-HSDs: adrenal, testis, ovary
=17β-HSDs: testis, ovary
=5a-reductases: testis & peripheral tissues

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9
Q

How is testosterone made?

A

-DHEA & androstenedione made in BOTH male & female gonads
-Same pathway as adrenal gland
-BUT ovaries & testis Leydig cells contain an additional enzyme:
=17β-hydroxysteroid dehydrogenase-3 (17β-HSD-3)
=Converts androstenedione (‘pro’, precursor) to weak C19 androgen testosterone
=In testis Sertoli cells 5α-reductase converts testosterone to strong androgen 5α-dihydrotestosterone

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10
Q

How is oestradiol made?

A
  • 3β-HSD converts pregnenolone into progesterone in corpus luteum
  • In ovary & peripheral tissues, aromatase converts testosterone to strong oestrogen oestradiol (C18)
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11
Q

Describe the HP Gonadal axis in regulating sex steroid hormone synthesis

A

-Gonadotrophin-releasing hormone (GnRH) from HP preoptic nucleus
-Acts on anterior pituitary gonadotrophs:
=follicle-stimulating hormone (FSH)
=luteinizing hormone (LH)

-FSH and LH stimulate sex steroid hormone production in gonads
=androgens (male),
=oestrogens (female)
=ALSO inhibins (male & female)

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12
Q

Describe testis anatomy

A
  • Steroidogenic Leydig cells= make testosterone, regulated by LH
  • Sertoli cells= ‘nursery’ cells for sperm production make inhibin (key marker of cell function) and ABP (androgen binding protein), regulated by FSH
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13
Q

How does the Leydig and Sertoli cells interact?

A
  • LH stimulates testosterone (T) production by Leydig cells
  • FSH promotes inhibin & androgen-binding protein (ABP) in Sertoli cells
  • T moves from Leydig to Sertoli cells
  • T converted to DHT & binds to ABP in luminal fluid of the seminiferous tubules= locally very high concentration of testosterone to drive spermatogenesis and maturation
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14
Q

Where does testosterone act on?

A
  • T from Leydig cells & inhibin from Sertoli cells feedback on GnRH, LH & FSH
  • Testosterone transported in plasma to peripheral targets bound (98%) to sex hormone-binding globulin (SHBG)- concentrations of this protein regulated, disturbed in drug therapy (infertility)
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15
Q

What are the actions of androgens?

A
  • Testosterone, 5a-DHT
  • Primary male reproductive function= spermatogenesis, prostate secretions
  • Secondary male sex characteristics= anabolic (build muscle), deep voice, facial and body hair, brain (libido and aggression)
  • Essential during foetal life= male sex determination (week 7-8), genital development
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16
Q

How does testosterone influence male sex determination?

A
  • Foetus programmed to be female
  • Jolt of testosterone at week 7-8
  • SRY (sex determining gene on Y chromosome) = Sertoli cell differentiation = testis formation= Leydig cells develop to make T
17
Q

How in mice can you prove androgens have an essential role in male sex determination?

A

-Androgen Insensitivity syndrome
=due to mutated testosterone receptor:
-Arrested testis development; lack of testosterone & anti-Mullerian hormone
=lack of Mullerian duct regression
=Externally female as testis did not develop

18
Q

How does Androgen Insensitivity syndrome present in humans?

A

-46, XY genotype, variable phenotype

-Partial insensitivity:
=male external genitalia & body shape & mild spermatogenic defect after puberty
-Complete insensitivity:
=Female external genitalia & body shape, female internal organs undeveloped or absent

19
Q

Why are oestrogens essential in males?

A

-Not as much as females
-Aromatase converts to oestradiol in periphery and testis
-If failure to convert, oestrogen deficiency affects bone maturation
=tall and long arms
=bone epiphyses do not close in adolescence
=loss of bone mass
=osteoporosis= bone fractures
=slowed mineralization of bones (delayed bone age) =abnormally high blood sugar (hyperglycemia) because the body does not respond correctly to the hormone insulin.
=excessive weight gain and a fatty liver.

20
Q

Describe aromatase deficiency in females

A

=born with external genitalia that do not appear clearly female or male (ambiguous genitalia).
=These individuals typically have normal internal reproductive organs, but develop ovarian cysts early in childhood, which impair the release of egg cells from the ovaries (ovulation).
=In adolescence, most affected females do not develop secondary sexual characteristics, such as breast growth and menstrual periods.
=They tend to develop acne and excessive body hair growth (hirsutism).

21
Q

Describe aromatase deficiency in males

A

-Some men with this condition have decreased sex drive, abnormal sperm production, or testes that are small or undescended (cryptorchidism)

22
Q

How does aromatase deficiency of foetuses affect the pregnancy?

A
  • Women who are pregnant with foetuses that have aromatase deficiency often experience mild symptoms of the disorder even though they themselves do not have the disorder.
  • These women may develop hirsutism, acne, an enlarged clitoris (clitoromegaly), and a deep voice. These features can appear as early as 12 weeks of pregnancy and go away soon after delivery.
23
Q

Describe the way oestrogens are made in the ovaries

A

-LH stimulates production of androstenedione & testosterone in thecal cells of the primary follicle
-Androgens move from thecal to granulosa cells
-FSH stimulates androgen conversion to oestrogens by aromatase
=regulates proliferative phase of menstrual cycle

24
Q

How does oestradiol travel in the body and feedback?

A
  • Oestradiol & inhibin from granulosa cells feed back on GnRH + LH & FSH release from HP & pituitary
  • Oestradiol also transported in plasma, to peripheral targets bound to gonadal sex hormone-binding globulin (SHBG)
25
Q

What are the actions of oestradiol?

A
  • Female genital development & differentiation
  • Secondary female sex characteristics, e.g. body fat distribution, cardiovascular system, skin, bone, epiphyseal closure
  • Estrogen from the primary ovarian follicle promotes endometrial growth during the follicular or ‘proliferative’ phase (thicker)
26
Q

What are the actions of progesterone?

A
  • Made in the corpus luteum promotes endometrial secretion & vascularisation during the luteal or ‘secretory’ phase
  • Prepares uterus for implantation of a fertilised egg
  • Without implantation falling progesterone initiates menstruation
27
Q

What are the phases of the ovarian cycle?

A
  • Follicular/ proliferative phase (Day 0-14)
  • LH surge triggering ovulation (Day 14)
  • Luteal/ secretory phase (Day 14-28)
28
Q

Describe the follicular/ proliferative phase

A
  • FSH & LH stimulate oestradiol production by the primary follicle
  • promotes endometrial growth by proliferation
29
Q

Describe the LH surge triggering ovulation

A

-Estrogen is produced by the granulosa cells of the developing follicle andexertsnegative feedback on LH production in the early part of the menstrual cycle via the HPG axis.
=However, once Estrogen levels reach a critical level as oocytes mature within the ovary in preparation for ovulation, Estrogen begins to exert positivefeedback on LH production, leading to the LH surge= stimulates ovulation (follicle ruptures and releases egg which then makes oestrogen)

30
Q

Describe the luteal/ secretory phase

A
  • corpus luteum makes progesterone

- receptive ‘secretory’ environment for implantation of a fertilised egg

31
Q

What happens if no implantation occurs during the normal ovarian cycle (day 14-28)?

A

-corpus luteum regresses & stops producing progesterone

  • declining feedback of :
    • progesterone
    • oestrogen
    • inhibin
  • allows a new cycle of LH & FSH release
32
Q

What happens if implantation occurs during the normal ovarian cycle (day 14-28)?

A

-Developing embryo produces hCG (human chorionic gonadotrophin) an alternative form of LH (with sugar group)
-hCG binds to LH receptors on corpus luteum & endometrium:
=maintains progesterone secretion
=suppresses maternal immune rejection of placenta
-progesterone promotes uterine blood vessels to sustain the growing fetus

33
Q

Describe the luteal-placental shift

A

-Occurs at 7-9 weeks
-Hormones decline:
=hCG from embryo
=progesterone from corpus luteum
-To maintain pregnancy, placenta begins to produce:
(i) progesterone from cholesterol
(ii) oestrogen from DHEA (foetal adrenal)

Endocrine & Diabetes (45 decks)

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