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Biol 432 > Endocrinology of Male and Female Reproductive Systems > Flashcards

Endocrinology of Male and Female Reproductive Systems Flashcards

1
Q

Testes (in terms of steroli/leydig cells)

A

•both steroli and leydig cells support each other so spermatogenesis can occur – want cooperativity between these two cell types

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2
Q

Leydig cells

  • what are they
  • what do they secrete
  • what do they support
A
  • interstitial cells
  • major endocrine tissue
  • secrete testosterone
  • support the growing spermatogonium to produce mature sperm cells
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3
Q

Steroli cells

  • what are they part of
  • what do they contribute to
  • what do they secrete
A
  • part of seminiferous tubules
  • spermatogenesis
  • form blood-testis barrier
  • secrete ABP (androgen-binding protein) facilitate spermatogenesis (helps ferry spermacytes)
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4
Q

17 a hydroxylase is most active in which cell types

A

leydig cells

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5
Q

what is 5a reductase important for

A

maintain androgen effects such as tallness of an organism, strength of bones, deptheness of voice etc

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6
Q

what is aromatase important for

A

important target in chemotherapy against breast cancer and converting androgens into estrogens (making ring aromatic)

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7
Q

The testosterone axis

A

GnRH (Hypothalamus) to LH (Pituitary) to Testosterone: produced by Leydig cells in testes (which also produce Androstenedione and DHEA)
•need 5 alpha reductase to convert testosterone into DHT
•specialialized cells in ovary also produce androstenedione and DHEA

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8
Q

testosterone functions (3)

A
  • normal spermatogenesis
  • secondary sexual characteristics (muscle, voice, testes, hair and increase prostate)
  • anabolic effects on muscle liver and kidney (effects on enzymes)
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9
Q

testosterone levels in blood depend on what 3 things

A
  1. steroidogenic abilities of individual Leydig cells
  2. total number of Leydig cells per testes
  3. LH levels (which depends on GnRH)
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10
Q

where is sex hormone binding globulin (SHBG) synthesized

A

in the liver

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11
Q

in the blood what is testosterone bound by

A

bound by albumin (38%) or sex hormone binding globulin (60%) SHBG

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12
Q

testosterone action on target cells

  1. T bound by ____
  2. free T….
  3. T reduced to ___ by _____ or aromatized to _______
A
  • Circulating testosterone bound by sex hormone binding globulin (SHBG)
  • Free T enters the cell
  • Either testosterone is reduced to DHT by 5 alpha reductase or aromatized to estradiol (E2) – aromatase is a cytP450 type enzyme and can be upregulated by EDCs
  • DHT and T bind same R
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13
Q

Hypothalamic pituitary axis (leydig cells) 3 points

A
  • LH binds LHR via GPCR GaS which increases AC, increases cAMP and leads to increase amount of steroidogenic acute regulatory protein (StAR) which stimulates path for T synthesis and release
  • Negative feedback by estradiol and testosterone
  • Positive feedback by activin to increase FSH
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14
Q

Hypothalamic pituitary axis (steroli cells) 2 points

A
  • Have a lot of receptors for FSH – increase amount of androgen binding protein which is helping spermatogenesis
  • FSH binds FSHR via GPCR GaS which increases Ac, increases cAMP and leads to increase in ABP which increases concentration of intratubular testosterone and facilitates spermatogenesis
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15
Q

what is mulerian inhibiting factor (MIF) important for

A

•important in gonadal differentiation and also TGF beta family

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16
Q

what does inhibin do and where is it produced

A
  • Inhibits FSH secretion from pituitary (not LH) – won’t inhibit LH produced by steroli cells in males
  • Produced by Steroli cells (male) late granulosa (inhibin B) and corpus luteum (inhibin A) (female)
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17
Q

what does activin do and where is it produced

A
  • Activates FSH secretion and binding (via positive feedback)
  • Produced by Leydig cells (male) early granulosa cells or late corpus luteum (female)
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18
Q

are activin and inhibin hetero or homodimers of alpha/beta subunits

A

activin: heterodimers and homodimers of beta subunits
inhibin: heterodimers of alpha and beta subunits

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19
Q

what does follistatin do

A

•Binds activin, decreases bioavailability and decreases FSH synthesis

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20
Q

what hormone is produced in the ovary and what does it do

A

•Estrogen – secondary sexual characteristics (voice, body type, breasts etc.) and stimulate uterus & ovary size and development

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21
Q

what are granulosa cells composed of and what do they lack

A
  • Estradiol and activin
  • Lack 17a-hydroxylase (no androgens) despite producing a lot of estradiol – so need a partner (coming from the theca cells) known as 2 cell hypothesis
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22
Q

what do theca cells produce

A

androstenedione which can easily pass through membrane and is used as a precursor to make estrogens (estrogens are important in all cells for growth)

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23
Q

what do theca cells lack

A
  • Lack aromatase (no estradiol E2)

* No FSHR (no FSH receptors but have LH receptors like the Leydig cells)

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24
Q

Two cell hypothesis (preovulatory follicle) - what is the major product

A

•major product is androstenedione which will support production of estradiol in particular phases (estradiol is higher in pre-ovulatory phase - in first 10-12 days of the 30-day cycle)

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25
Q

two cell hypothesis (preovulatory follicle) - theca cell part

A

•Because Theca cells have LH receptors they increase production of cAMP and that will stim a lot of things including TF SF-1 which increases production of 17a hydroxylase in the nucleus and maintenance of STAR then will go to smooth ER where androstenedione is produced and delivered in high quantities to produce estradiol
•Also increase in cAMP and SF-1 will increase amount of P450 aromatase so we can get production of estradiol
*SF-1=steroidogenic factor 1 (transcription factor)

26
Q

the two cell hypothesis (corpus luteum) what is different from the preovulatory follicle stage

A

Granulosa cell still being supported by FSH to its receptor but has been an upregulation of LH receptors *diff from last stage so both FSH and LH will increase at ovulation

27
Q

why is the corpus luteum such an important phase

A

because it can potentially support a pregnancy and fertilization of mature ova

28
Q

what hormone levels will decrease in the corpus luteum phase

A

estrogen

29
Q

Follicular phase (GnRH)

A

initially a slow pulse frequency – The increase of activin favours FSH release over LH (but still stimulates LH release)

30
Q

Follicular phase (FSH)

A

increase of E2 from granulosa cells

  • E2 (alone) – negative feedback on hypothalamus and pituitary – initially decreases the amount of GnRH released BUT later increases GnRH pulse frequency which lowers FSH relative to LH
  • Therefore, E2 causes increase in GnRH pulse frequency – favours LH and Follistatin
31
Q

luteal phase what occurs (3)

A

•Corpeus luteum: increase in progesterone and negative feedback on GnRH (pregnancy too)

  • increase inhibin A = decrease in FSH
  • Later in the phase higher LH levels (relative to FSH) increase activin = increase FSH to restart cycle
32
Q

cessation (no implant - luteolysis)

A

Decrease E2 and progesterone and inhibin (LHR downregulated on follicular cells) and prostaglandins cause vasoconstriction and relaxation = menstruation

33
Q

what is follicular development fostered by

A

FSH which results in E2 production and causes positive feedback to produce LH surge
-estradiol peak during follicular phase

34
Q

what occurs after ovulation

A

the corpus luteum produces progesterone causing a slowing of GnRH pulse generator and decease in LH

35
Q

what hormone is high in the first 10 days of the menstrual cycle vs the luteal phase

A

first 10 days is high levels of estrogen and in luteal it is progesterone

36
Q

the pulsatile secretion of GnRH from the hypothalamus occurs at what rate to be essential for maintenance of the menstrual cycle

A

one pulse per hour

37
Q

what are the GnRH pulses due to

A

oscillations in the electrical activity of the GnRH pulse generator in the hypothalamus

38
Q

what does the GnRH pulse generator invovle (in terms of hormones)

A

GnRH pulse-generator seems to involve both norepinephrine and kisspeptin as well as components of the circadian clock – kisspeptin neurons are receptive to estrogen levels

39
Q

what activates kisspeptin neurons (GnRH pulse generator)

-what is the final outcome with this

A

• Increasing estrogen production activates kisspeptin neurons overriding the normal tonic repression by ovarian steroids and increasing GnRH pulse frequency and amplitude
-results in LH synthesis leading to LH surge and triggering ovulation

40
Q

what external condtitions can effect the activity of the pulse generator

A

• A number of conditions such as stress, light changes, exercise and sleep affect the activity of this pulse generator

41
Q

do changes in body fat affect menstrual cycles (if so, explain)

A

yes, Changes in body fat levels will affect menstrual cycles and level of visceral fat since it affects aromatase – studies have shown that pulse generator activity is also maintained by specific metabolic signals meant for energy homeostasis

42
Q

what second messenger stimulates GnRH release

A

Increased cyclic AMP (cAMP) levels in neurons appear to stimulate GnRH release by activation of cAMP-gated cation (Cyclic nucleotide-gated ion channels: CNG) channels

43
Q

activation of cyclic nucleotide gated ion channels (CNG) correlate with what

A

Activation of the CNG channels correlate with increase neuron excitability and calcium oscillations

44
Q

what would negative feedback pathways do to cAMP

A
  • Potential negative feedback pathways may decrease cAMP levels by inhibiting AC 5 and activating phosphodiesterase
  • These stimulatory and inhibitory cAMP-signalling pathways appear to regulate the excitability of these neurons and many constitute a biological clock timing the pulsatile release of GnRH
45
Q

How is the LH surge toned down?

hint: it is a attenuating factor

A
  • Gondadotropin surge-attenuating factor (GnSAF) is a non-steroidal ovarian hormone produced by granulosa cells
  • GnSAF is involved in regulating the secretion of LH form the anterior pituitary
  • Higher levels of progesterone also contribute to negative regulation of GnRH
46
Q

what stimualtes our desire to eat vs inhibits it

A

Neuropeptide-Y stimulating our desire to eat and Cholecyrokinin is inhibiting
-leptin also has an affect

47
Q

what neurotransmitter has a negative effect on GnRH producing neurons

A
  • Serotonin negative effect on GnRH producing neurons – lots produced during daytime
  • ANP, prolactin and MSH all also having negative effects
48
Q

what neurotransmitter has a positive effect on GnRH producing neurons

A

acetylcholine

49
Q

what is atresia

A

•Atresia is a condition in which a particular cell type that lines a passage or makes up a tissue in the body is abnormally closed or absent

50
Q

what is follicular atresia

A

apoptosis of ovarian follicles

51
Q

what is follicular atrisia inhibited by

A

FSH (since FSH stimulates follicle growth)

-once follicile has developed it secretes estrogen which in high levels decreases secretions of FSH

52
Q

why is ovarian cell death an essential process

A

•Ensures the selection of the dominant follicle and the demise of excess follicles (follicle = egg plus surrounding cells)
Minimizes the possibility of multiple embryo development during pregnancy and assures the development of few but healthy embryos – only 0.1% of the approximate

53
Q

what anti-apoptotic factors are invovled in follicular atresia

A

anti-apoptotic factors: FSH, LH, P, IGF-1, EGF, basic fibroblast growth factor (bFGF), transforming growth factor alpha (TGFa), TGFb, activin, insulin, T and GnRH

54
Q

which pro-apoptotic factor are involved in follicular atresia

A

tumor necrosis factor alpha (TNFa)

55
Q
  1. what protects from atresia in terms of hormone level balance
  2. in terms of IGF-1
A
  • When the level of estradiol and the ratio of estradiol to progesterone is high it protects from atresia
  • The level of IGF-1 in potentially dominant follicles (healthy follicles) is higher than in atretic follicles
  • The expression of IGF receptor is decreased in atretic follicles as compared to that in healthy follicles
56
Q

what is atresia initiated by

A

by granulosa cell apoptosis

57
Q

what is granulose cell apoptosis promoted by

A

•promoted by TNF alpha and includes other pro-death factors such as FAs and TRAIL

58
Q

what causes apoptosis?

A
  • During mammalian ovarian follicular development only limited numbers of follicles are selected for ovulation – the rest undergo atresia
  • About 20 follicles mature each month but only a single one is ovulated – the follicle form which the oocyte was released becomes the corpus luteum and the rest undergo atresia
59
Q

what is the most prevalent female endocrinopathy and the largest single cause of infertility

A

Polycystic ovarian syndrome (PCOS)

60
Q

what is PCOS characterized by

A
  • Characterized by multiple small follicles arrested in their development but nonatretic
  • Hyper-expression of antiapoptotic factors growth factors (e.g. EGF/TGFa) blocks apoptosis and atresia, leading to an accumulation of multiple small follicles

Biol 432 (11 decks)

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