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HPG axis Flashcards

1
Q

LH/FSH structure

A

α subunit common to all glycoprotein hormones
β subunits differ and confer specificity and biological activity
subunits have no biological activity when separate

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2
Q

causes of hypothalamic amenorrhoea

A

functional: weight loss, exercise, stress

GnRH deficiency: Kallman’s syndrome, idiopathic

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3
Q

Tx of hypothalamic amenorrhoea

A

pulsatile GnRH

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4
Q

inhibin A vs inhibin B

males/female production, function

A

males: no inhibin A, inhibin B produced by sertoli cells and inhibits FSH secretion (negative feedback)
females: produced by granulosa cells, inhibin B rises in early follicular phase, inhibin A (more dominant) in mid-late follicular phase and peaks at mid-luteal phase

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5
Q

where is testosterone produced

A

males: leydig cells of testis
females: ovary and adrenal cortex

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6
Q

functions of testosterone (in males and females)

A

males: spermatogenesis, development of secondary sexual characteristics (facial hair, muscle mass, change in voice etc.)
females: biosynthesis of oestrogens

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7
Q

where is progesterone produced

A

corpus luteum + placenta

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8
Q

functions of progesterone

A

maintenance of endometrium, implantation and maintenance of pregnancy

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9
Q

different types of oestrogens (3)

A

E1: oestrone, main oestrogen of menopause
E2: oestradiol, most bioactive, preparation of uterus + reproductive tract for conception + pregnancy
E3: oestriol, main oestrogen of feto-placental unit

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10
Q

where are oestrogens produced

A

ovary, growing follicles, corpus luteum, adipose tissue, placenta

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11
Q

function of kisspeptin

A

controls GnRH synthesis and secretion
central and peripheral administration increases LH, FSH and testosterone (dose-dependent)
studies showed that kisspeptin increased number of LH pulses and pulse amplitude

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12
Q

functions of LH (F: 4 / M: 1)

A

females: androgen production by thecal cells
remodelling of follicle to remnant corpus luteum
corpus luteum progesterone production
ovulation
males: testosterone production by leydig cells

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13
Q

functions of FSH (F: 2 / M: 1)

A

females: conversion of androgens to oestrogens by granulosa cells
follicular maturation
males: sertoli cell metabolism

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14
Q

what receptor does kisspeptin bind to

A

GPR54, found on GnRH neurons

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15
Q

how is oestrogen -ve/+ve feedback mediated (in rodents)

A

low levels: arcuate nucleus (-ve)

high levels: kisspeptin neurones in AVPV (+ve)

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16
Q

GnRH pulse freq and amplitude in males vs females

A

males: constant freq every 2hrs
females: high freq (every 30min) -> LH
low freq and amplitude (every 90-120min) -> FSH

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17
Q

GnRH pulses during menstrual cycle

A
  1. early follicular phase: slow pulses -> FSH
  2. mid-late follicular phase: increased freq -> LH
  3. after ovulation: pulses decrease -> FSH production
  4. end of luteal phase: pulses increase -> FSH secretion
18
Q

GnRH intracellular signalling

A

binds to GnRHR (GPCR) -> Gαs and q -> cAMP -> MAPK -> LHβ and FSHβ genes -> GnRH transcription, translation & secretion via exocytosis

19
Q

FSH intracellular signalling

A

FSH binds to FSHR -> exchange of GDP for GTP -> dissociation of Gα from βγ -> adenylate cyclase -> cAMP -> PKA -> downstream phosphorylation, further kinase activation -> cellular responses

20
Q

regulation of FSH receptor signalling

A

receptor activation -> activation of G-protein regulatory kinases -> phosphorylation of residues on intracellular loops -> βarrestin targets receptors for endocytosis in clathrin-coated pits -> dynamin pinches off endocytotic vesicles -> receptor undergoes lysosomal degradation or recycling to membrane

21
Q

inhibin: produced where? function?

A

produced by sertoli cells

decreases FSH secretion from pituitary

22
Q

activin: produced where? function?

A

produced by sertoli cells

increases FSH secretion from pituitary

23
Q

cause of familial hypogonadotrophic hypogonadism

A

GnRH frameshift mutation

24
Q

Kallman syndrome: pathophysiology -> presentation

A

failure of migration of hypothalamic neurones from medial olfactory placode to medio-basal hypothalamus -> loss of hypothalamic GnRH secretion
HH + anosmia + delayed/no puberty

25
Q

LHbeta mutation -> ? in females vs males

A

females: anovulatory infertility
males: loss of testosterone -> impaired sexual maturation

26
Q

FSH receptor mutation -> ? in females vs males

A

females: arrested follicular maturation
males: reduced fertility, poor sperm quality

27
Q

differences in LH KO in mice and humans

A

KO of pituitary LH in humans → hCG still produced which can bind to LHR → testosterone → male differentiation
KO of LHR -> loss of LH and hCG effects
KO of pituitary LH in mice -> compensation by paracrine factors

28
Q

evidence for kisspeptin action being mediated via GnRH

A

kisspeptin causes depolarisation of GnRH neurones in vitro

kisspeptin stimulated LH secretion dependently from hypothalamic explants

29
Q

what gene and receptor for neurokinin B

A

TAC3

NK3R

30
Q

where are neurokinin B neurones found

A

hypothalamus (particularly arcuate nucleus), basal forebrain

31
Q

neurokinin B action

A

NK binds to NK3R on kisspeptin neurones (project to GnRH neurones) -> kisspeptin release -> GPR54 on GnRH neurone -> augments GnRH synthesis and/or release

32
Q

evidence for kisspeptin effects on LH

A

anti-kisspeptin Ab -> loss of LH surge in rats

33
Q

Jost paradigm

A
  1. chromosomal
  2. gonadal
  3. hormonal
  4. phenotypic
  5. behavioural
34
Q

sexual differences in HPG axis (5)

A
  1. larger anteroventral periventricular nucleus in females (as needed for GnRH/LH surge)
  2. M always respond to kisspeptin / women most sensitive to kisspeptin during preovulatory phase
  3. AVPV kisspeptin neurones in F only, ARC kisspeptin in both
    - organisational effect (neuro-anatomical difference)
  4. oestrogen/testosterone in utero in F -> fewer AVPV
    castration in M -> development of AVPV kisspeptin neurones
  5. in F high E2 in preovulatory phase -> increased sensitivity to GnRH - activational effect (reversible)
  6. may be difference in neurokinin B but currently unclear
35
Q 
effects of:
1. ghrelin
2. PYY
3. leptin
on reproductive activity
A
  1. ghrelin suppresses
  2. PYY enhances
  3. leptin enhances
36
Q

mechanism of leptin enhancement of HPA

A

leptin activates GnRH neurones via kisspeptin or via glutamate (in ventral premamillary nucleus)
therefore puberty can occur even w leptin KO

37
Q

hormonal changes at puberty

A

LH + FSH -> testes development, follicle development, menarche
oestrogen -> female secondary sex characteristics
testosterone -> male secondary sex characteristics
DHEAS -> pubic and axillary hair growth
inhibin produced from sertoli / granulosa cells
GH -> growth spurt
prolactin -> breast development

38
Q

mechanism for increased FSH during and after menopause

A

decreased ovarian reserve of follicles -> decreased E2 and increased FSH -> multiple antral follicles / follicular cysts -> E2 -> FSH suppression
after menopause too few follicles to respond to FSH

39
Q

causes of decreased fertility w age (4)

A

occurs 10 years before menopause
decreased ovarian reserve (by ovulation and attrition)
increased chromosomal abnormalities
hypothalamus less sensitive to E2
decreased coital freq -> oocyte spends more time in repro tract

40
Q

causes of secondary amenorrhoea (2)

A

PCOS

hypothalamic hypogonadism: functional, Kallman’s, prolactinoma or other pituitary tumour

41
Q

GnRH structure (7)

essay topic

A
  1. Primary structure: 10 amino acids
  2. Horseshoe structure
  3. Synthesised as pre-prohormone: signal peptide, GnRH decapeptide, link and GAP peptide
    GnRH and GAP co-secreted; function of GAP unknown
  4. N-terminus: receptor binding and activation
  5. C terminus: receptor binding only
  6. Central arginine often modified to give agonistic/antagonistic effects
  7. L to D-amino acid (resistant to proteolytic degradation) substitutions → long half-life in blood

rds (13 decks)

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