Appetite regulatiom Flashcards
when do you feel thirst
increase in osmolarity
reduced blood vol
reduced bp
what is more significant for thirst - bp/osmolarity
osmolarity
describe the action of ADH
act on kidneys
regulate vol and osmolarity of urine
low ADH = water diuresis - large vol of urine
high ADH = anti diuresis
describe urine osmolarity
Sacrifice urine osmolrity to preserve blood osmolarity
where are osmoreceptors found
Organum Vasculosum Laminae Terminalis
hypothalmus
subfornical organ
describe the Organum Vasculosum Laminae Terminalis and subfornical organ
???
Circumventricular organ – not protected by bb brain –so that the brain can sence what is going oin in circulation
purpose of the blood brain barrier
Blood brain preserve brain from normal blood func – selectively allow what enters
action of osmoreceptors
sense changes in blood osmolarity
Shape change changes the way they signal
Shrink – signal to ADH producing cells – produce ADH
swell- stop ADH release
Same signal for thirst – tell cns need to drink
effect of increased plasma osmolarity
- drink
- ADH release - conserve more water
effect of decreased plasma osmolarity
thirst and ADH suppressed
excrete more water
describe the sensation of thirst
decreased by drinking before sufficient water is reabsorbed
because of receptors in mouth, pharynx, oesophagus
relief is short lived
If then suck water out of stomach – system knows been fooled and thirst comes back if water doesn’t enter circulation
relief only completely satisfied when osmolarity, bp or vol corrected
describe the renin-angiotensin-aldosterone system
liver -> angiotensiongogen -> ang1 (renin catalyse) -> ang2 (ACE catalyse) -> aldosterone from zona glomerulosa
describe how the renin-ang-ald system affects thirst
ANG2 –adrenal – aldosterione
Absorb salt to absorb water
Same system for thirst
ANG2 = thirst as well as other effects
describe ANG2
increased when blood vol and bp reduced
activates SFO neurons
restore fluids
where does excess energy intake go
adipose away
describe body weight homeostasis
signals are integrated in the hypothalamus
signal from ghrelin, PYY
neural input from periphery (vagus if stomach stretched) and other regions of brain
leptin
output - food intake, energy expenditure
circuits in the brain for appetite regulation
signals from periphery to hypothalamus, integrate -> higher centres - actually perform the actions ie eat or move more
redundancy - difficult to eat if not hungry
which part of the hypothalamus is involved in regulating food uptake
arcuate nucleus
describe the arcuate nucleus
circumventricular - incomblete bb barrier
integrate peripheral and central feeding signals
stimulatory - NPY/Agrp
inhibitory - POMC
the relationship between the 2 neuronal populations in the arcuate nucleus
Completely separate populations – don’t want overlap of accelerator and break
organisation of the neural populations in the arcuate nucleus and how they act
hormones bind to receptors on neurons’ cell bodies in the arcuate nucleus - axons go all over the brain eg - paravent nucleus - synapse here and go downstream abd cause other effects
regulate TH release as well - regulate metabolism
describe the melanocortin system
MCR4 – concentrated in hypothamus (paraventricular nucleus) and areas of food intake - reduces food intake
POMC and agrp are released from the arcuate nucleus
POMC -> A-MSH -> inhibit food intake
by binding to MC4R
Agrp – antagonist of the same receptor, this is a rare endogenous antagonist – when hungry this receptor is blocked
effect of no POMC or MC4R
put on a lot of weight
don’t cause the high obesity prevalence but important in signalling
effect of NPY/agrp
increase food intake
are they known mutation in NYP or agrp related to appetite in humans
no
other brain regions involved in appetite regulation
Higher centres - dieting
Amygdala- emotion, memory.
Other parts of the hypothalamus, e.g. lateral hypothalamus
Vagus to brain stem to hypothalamus - info about mechanical distension
describe the adipostat mechanism
circulating hormone produced by fat
hypothalamus senses the concentration of hormone
alter the neuropeptides - alter food intake
Principle: Regulate body weight depending on how much body fat you had
Problem with this mechanism – that’s why people put on weight
describe leptin
made by adipocytes in white adipose tissue
circulates in plasma
act on hypothalamus - regulate appetite and thermogenesis (expenditure)
high = high fat low = low fat
3 possible disruption sto the leptin pathway that cause people to get obese
People get obese – don’t have leptin = no signal
Leptin not regulated – no more produced when you put in weight
Hypothalamus – it is released but doesn’t signal effectively
which disruption to leptin is the case
Fat – more adipose – more leptin – doesn’t signal effectively – have leptin resistance
high fat diet reduces sensitivity to leptin
people with a mutated version of leptin
obese
Have mutated version of leptin – so never seen it before – for these children it is really important
They feel like they’re starving to death – food should be a priority – one mutation of a particular gene – powerful mutation
leptin effective at reducing body weight
what is it that makes you feel less hungry after a meal
hormonal signal from gut
which cell are PYY and GLP1 released from
L cells
which part of PYY is involved in appetite regulation
aa 3-36
action of PYY
modulates neurons in arcuate nucleus
inhibit NPY
stimulate POMC
decreases appetite
Tell brain you’ve ad calorie load so you should feel full – stop for a while
describe the structure of Ghrelin
28aa
FA chain attached - travel in circ - how bind to receptor
role of ghrelin
drive the anticipation of food and hunger
action of ghrelin
Stimulates NPY/Agrp neurons.
Inhibits POMC neurons.
Increases appetite - and food intake
affect of adding Ghelin to rats
Fool body to think it is fasting – make think nutritional state is different
gut hormones as a treatment of obesity
novel
target only relevant circuits
released daily - no side effects
Wouldn’t ware off because go throughout live nbormally
GLP1 analogue
GLP1 suppress appetite
approved for diabetes and obesity = few Kg weight loss
how can we tell that the obesity epidemic is not just related to genetics
it has happened to fast for a change in genetics
what is responsible for the epidemic
Thing that has changed is the env, food is cheap – wages for food is the lowest its been
Environment has changed – so the effect on genetics has changed
Small changes in many genes contribute to body weight
