Fuel homeostasis and reproduction function Flashcards
how would you describe the interaction between fuel homeostasis and reproductive function
bi-directional
why is nutrition status relevant to reproductive function
reproduction requires a lot of energy
what effect does obesity have on reproductive function
impairs it
what effect does fasting have on reproductive function
impairs it
how does fasting impair reproductive function
- regular LH pulses become disrupted
- low leptin levels means POMC isnt stimulated and NPY isnt inhibited
what does low levels of POMC mean for reproduction
low POMC means GnRH and kisspeptin arent stimulated and so puberty isnt stimulated
what does high NPY mean for reproduction
inhibits GnRH and kisspeptin and so puberty isnt stimulated
how does leptin help reproductive function
in normal state, leptin levels are sufficient to stimulate POMC and inhibit NPY
this combination aloows GnRH and kisspeptin to stimualte puberty
what inhibits GnRH and kisspeptin
High NPY and low POMC
How is LH affected by obesity
pulses of LH keep their frequency by their amplitude is reduced
how does obesity affect reproduction
- LH surges are smaller
- leptin resistance develops which means POMC is low and NPY is high
main signalling mechanisms for communcating health energy status to HPG axis
leptin
other signals involved in energy homeostasis
insulin, ghrelin, PYY
under normal circumstances how does reproductive function effect fuel homestasis
very little effects, just slight changes in insulin sensitivity and energy homesostasis across the female reproductive cycle and at puberty
when does reproductive function have an effect on fuel homeostasis
pregnancy - reproductive axis has a big effect on energy homeostasis
Why does pregnancy effect energy homeostasis
there are many circulating hormones and signals involved in pregnancy. All women become insulin resistance during pregnancy
when is it normal for insulin resistance to occur
pregnancy
when does insulin resistance have protective effects
pregnancy
how does insulin resistance occur in pregnancy
post receptor signalling is inhibited by progesterone and cortisol
is inuslin binding affected in pregnancy
no. although progesterone and cortisol inhibit insulin binding, this is balanced by the stimulatory effects of oestrogen
what stimulates insulin binding
oestrogen
what inhibits insulin binding
progesterone and cortisol
is insulin resistance consistant in pregnancy
no, it increases across pregnancy when hormone levels increase
how is insulin resistance benificial
there is more glucose available for the foetus
how does foetus get glucose when mother has normal insulin sensitivity
some glucose in maternal blood is transported across placenta via GLUT3 transporters
transporter for glucose from maternal blood to placenta
GLUT3
What must adapt to maternal insulin resistance
Islet cells must adapt to prevent development of gestational diabetes
how do islets adapt to insulin resistance in pregnancy
- increased glucose-stimulated insulin secretion
- increased beta cell mass
- increased insulin synthesis
- increased gap junctions between beta cells
- increased cAMP synthesis
what tells islet cells to adapt to insulin resistance in pregnancy
prolatin and placental lactogen
where is prolactin released from
pituitary
functions of prolaction
regulates immune system, growth factor, anti-apoptopic, signals to islets to adapt
what does prolactin act on
PRL receptor
where is placental lactogen from
placenta
function of placental lactogen
stimulates development of mammary glands in late pregnancy and similar functions as prolactin
what does placental lactogen bind to
PRL receptor
what acts on the PRL receptor
prolactin and placental lactogen
what happens when islets fail to adapt to insuin resistanace in pregnancy
gestational diabetes
gestational diabetes is caused by
failure of the islet cells to adapt to insuin resistance in pregnancy
why is gestational diabetes a problem in pregnancy
risks to the mother and the baby
risks to mother from gestational diabetes
- high BP
- pre eclampsia
- UTI
- c-section
risks to baby from gestational diabetes
- macrosoia = big baby
- risk of birth injury
- hypoglycaemia
- respiratory problems
why doe some beta cells fail to adapt to insulin resistance
Not becuse of low levels of prolactin or placental lactogen becuase studies show levels are the same, although may be more resistance
risk factors for developing gestational diabetes
same as those of T2DM
- race
- high BMI
- age
- family history
why does fuel homeostasis matter during pregnancy
to supply foetus with eneryg for growth whilst keeping mother healthy
what other syndroms are strongly linked to insulin resistance and hyperinsulinemi in pregnancy
PCOS and hyperandrogenemia
insulin and LH
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
insulin and FSH
high insulin impairs action of FSH on granulosa leading to follicular arrest
how does excess androgens effect insulin
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
cycle of high androgens on insulin
high androgens = increased insuline resistance in muscle and adipose = increased plasma insulin
how is PCOS a viscous bi-directional cycle
PCOS is characterised by postive loop between androgens and insulin.
unsure which is the inial cause, but may be mutlple factors
what does hyperinsulinemia cause in terms of PCOS
- increased androgen release from theca cells
- impaired follicle development
- possible increased GnRH pulses
= hyperandrogenaemia
what does hyperandrogenaemia cause in terms of PCOS
- increased insulin resistance in muscle and adipose
= hyperinsulinemia
