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Endocrinology & Reproduction > Fuel homeostasis and reproduction function > Flashcards

Fuel homeostasis and reproduction function Flashcards

1
Q

how would you describe the interaction between fuel homeostasis and reproductive function

A

bi-directional

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2
Q

why is nutrition status relevant to reproductive function

A

reproduction requires a lot of energy

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3
Q

what effect does obesity have on reproductive function

A

impairs it

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4
Q

what effect does fasting have on reproductive function

A

impairs it

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5
Q

how does fasting impair reproductive function

A
  • regular LH pulses become disrupted

- low leptin levels means POMC isnt stimulated and NPY isnt inhibited

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6
Q

what does low levels of POMC mean for reproduction

A

low POMC means GnRH and kisspeptin arent stimulated and so puberty isnt stimulated

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7
Q

what does high NPY mean for reproduction

A

inhibits GnRH and kisspeptin and so puberty isnt stimulated

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8
Q

how does leptin help reproductive function

A

in normal state, leptin levels are sufficient to stimulate POMC and inhibit NPY
this combination aloows GnRH and kisspeptin to stimualte puberty

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9
Q

what inhibits GnRH and kisspeptin

A

High NPY and low POMC

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10
Q

How is LH affected by obesity

A

pulses of LH keep their frequency by their amplitude is reduced

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11
Q

how does obesity affect reproduction

A
  • LH surges are smaller

- leptin resistance develops which means POMC is low and NPY is high

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12
Q

main signalling mechanisms for communcating health energy status to HPG axis

A

leptin

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13
Q

other signals involved in energy homeostasis

A

insulin, ghrelin, PYY

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14
Q

under normal circumstances how does reproductive function effect fuel homestasis

A

very little effects, just slight changes in insulin sensitivity and energy homesostasis across the female reproductive cycle and at puberty

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15
Q

when does reproductive function have an effect on fuel homeostasis

A

pregnancy - reproductive axis has a big effect on energy homeostasis

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16
Q

Why does pregnancy effect energy homeostasis

A

there are many circulating hormones and signals involved in pregnancy. All women become insulin resistance during pregnancy

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17
Q

when is it normal for insulin resistance to occur

A

pregnancy

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18
Q

when does insulin resistance have protective effects

A

pregnancy

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19
Q

how does insulin resistance occur in pregnancy

A

post receptor signalling is inhibited by progesterone and cortisol

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20
Q

is inuslin binding affected in pregnancy

A

no. although progesterone and cortisol inhibit insulin binding, this is balanced by the stimulatory effects of oestrogen

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21
Q

what stimulates insulin binding

A

oestrogen

22
Q

what inhibits insulin binding

A

progesterone and cortisol

23
Q

is insulin resistance consistant in pregnancy

A

no, it increases across pregnancy when hormone levels increase

24
Q

how is insulin resistance benificial

A

there is more glucose available for the foetus

25
Q

how does foetus get glucose when mother has normal insulin sensitivity

A

some glucose in maternal blood is transported across placenta via GLUT3 transporters

26
Q

transporter for glucose from maternal blood to placenta

A

GLUT3

27
Q

What must adapt to maternal insulin resistance

A

Islet cells must adapt to prevent development of gestational diabetes

28
Q

how do islets adapt to insulin resistance in pregnancy

A
  • increased glucose-stimulated insulin secretion
  • increased beta cell mass
  • increased insulin synthesis
  • increased gap junctions between beta cells
  • increased cAMP synthesis
29
Q

what tells islet cells to adapt to insulin resistance in pregnancy

A

prolatin and placental lactogen

30
Q

where is prolactin released from

A

pituitary

31
Q

functions of prolaction

A

regulates immune system, growth factor, anti-apoptopic, signals to islets to adapt

32
Q

what does prolactin act on

A

PRL receptor

33
Q

where is placental lactogen from

A

placenta

34
Q

function of placental lactogen

A

stimulates development of mammary glands in late pregnancy and similar functions as prolactin

35
Q

what does placental lactogen bind to

A

PRL receptor

36
Q

what acts on the PRL receptor

A

prolactin and placental lactogen

37
Q

what happens when islets fail to adapt to insuin resistanace in pregnancy

A

gestational diabetes

38
Q

gestational diabetes is caused by

A

failure of the islet cells to adapt to insuin resistance in pregnancy

39
Q

why is gestational diabetes a problem in pregnancy

A

risks to the mother and the baby

40
Q

risks to mother from gestational diabetes

A
  • high BP
  • pre eclampsia
  • UTI
  • c-section
41
Q

risks to baby from gestational diabetes

A
  • macrosoia = big baby
  • risk of birth injury
  • hypoglycaemia
  • respiratory problems
42
Q

why doe some beta cells fail to adapt to insulin resistance

A

Not becuse of low levels of prolactin or placental lactogen becuase studies show levels are the same, although may be more resistance

43
Q

risk factors for developing gestational diabetes

A

same as those of T2DM

  • race
  • high BMI
  • age
  • family history
44
Q

why does fuel homeostasis matter during pregnancy

A

to supply foetus with eneryg for growth whilst keeping mother healthy

45
Q

what other syndroms are strongly linked to insulin resistance and hyperinsulinemi in pregnancy

A

PCOS and hyperandrogenemia

46
Q

insulin and LH

A

high insulin works with LH to stimulate theca cells to produce more androgens
this exacerbates the problem of antral cells already producing excess androgens in PCOS

47
Q

insulin and FSH

A

high insulin impairs action of FSH on granulosa leading to follicular arrest

48
Q

how does excess androgens effect insulin

A

normally, androgens and oestrogen balance eachother to allow for normal insulin binding. Excess androgens inhibit inuslin binding and so resistance occurs both in inulsin binding and in post-receptor signalling

49
Q

cycle of high androgens on insulin

A

high androgens = increased insuline resistance in muscle and adipose = increased plasma insulin

50
Q

how is PCOS a viscous bi-directional cycle

A

PCOS is characterised by postive loop between androgens and insulin.
unsure which is the inial cause, but may be mutlple factors

51
Q

what does hyperinsulinemia cause in terms of PCOS

A
  • increased androgen release from theca cells
  • impaired follicle development
  • possible increased GnRH pulses
    = hyperandrogenaemia
52
Q

what does hyperandrogenaemia cause in terms of PCOS

A
  • increased insulin resistance in muscle and adipose

= hyperinsulinemia

Endocrinology & Reproduction (15 decks)

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