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ailmentary > Appetite regulatiom > Flashcards

Appetite regulatiom Flashcards

1
Q

when do you feel thirst

A

increase in osmolarity
reduced blood vol
reduced bp

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2
Q

what is more significant for thirst - bp/osmolarity

A

osmolarity

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3
Q

describe the action of ADH

A

act on kidneys
regulate vol and osmolarity of urine
low ADH = water diuresis - large vol of urine
high ADH = anti diuresis

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4
Q

describe urine osmolarity

A

Sacrifice urine osmolrity to preserve blood osmolarity

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5
Q

where are osmoreceptors found

A

Organum Vasculosum Laminae Terminalis
hypothalmus
subfornical organ

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6
Q

describe the Organum Vasculosum Laminae Terminalis and subfornical organ
???

A

Circumventricular organ – not protected by bb brain –so that the brain can sence what is going oin in circulation

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7
Q

purpose of the blood brain barrier

A

Blood brain preserve brain from normal blood func – selectively allow what enters

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8
Q

action of osmoreceptors

A

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

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9
Q

effect of increased plasma osmolarity

A
  • drink

- ADH release - conserve more water

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10
Q

effect of decreased plasma osmolarity

A

thirst and ADH suppressed

excrete more water

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11
Q

describe the sensation of thirst

A

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

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12
Q

describe the renin-angiotensin-aldosterone system

A

liver -> angiotensiongogen -> ang1 (renin catalyse) -> ang2 (ACE catalyse) -> aldosterone from zona glomerulosa

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13
Q

describe how the renin-ang-ald system affects thirst

A

ANG2 –adrenal – aldosterione
Absorb salt to absorb water
Same system for thirst
ANG2 = thirst as well as other effects

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14
Q

describe ANG2

A

increased when blood vol and bp reduced

activates SFO neurons

restore fluids

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15
Q

where does excess energy intake go

A

adipose away

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16
Q

describe body weight homeostasis

A

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

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17
Q

circuits in the brain for appetite regulation

A

signals from periphery to hypothalamus, integrate -> higher centres - actually perform the actions ie eat or move more

redundancy - difficult to eat if not hungry

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18
Q

which part of the hypothalamus is involved in regulating food uptake

A

arcuate nucleus

19
Q

describe the arcuate nucleus

A

circumventricular - incomblete bb barrier
integrate peripheral and central feeding signals

stimulatory - NPY/Agrp
inhibitory - POMC

20
Q

the relationship between the 2 neuronal populations in the arcuate nucleus

A

Completely separate populations – don’t want overlap of accelerator and break

21
Q

organisation of the neural populations in the arcuate nucleus and how they act

A

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

22
Q

describe the melanocortin system

A

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

23
Q

effect of no POMC or MC4R

A

put on a lot of weight

don’t cause the high obesity prevalence but important in signalling

24
Q

effect of NPY/agrp

A

increase food intake

25
Q

are they known mutation in NYP or agrp related to appetite in humans

A

no

26
Q

other brain regions involved in appetite regulation

A

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

27
Q

describe the adipostat mechanism

A

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

28
Q

describe leptin

A

made by adipocytes in white adipose tissue
circulates in plasma
act on hypothalamus - regulate appetite and thermogenesis (expenditure)

high = high fat 
low = low fat
29
Q

3 possible disruption sto the leptin pathway that cause people to get obese

A

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

30
Q

which disruption to leptin is the case

A

Fat – more adipose – more leptin – doesn’t signal effectively – have leptin resistance
high fat diet reduces sensitivity to leptin

31
Q

people with a mutated version of leptin

A

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

32
Q

what is it that makes you feel less hungry after a meal

A

hormonal signal from gut

33
Q

which cell are PYY and GLP1 released from

A

L cells

34
Q

which part of PYY is involved in appetite regulation

A

aa 3-36

35
Q

action of PYY

A

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

36
Q

describe the structure of Ghrelin

A

28aa

FA chain attached - travel in circ - how bind to receptor

37
Q

role of ghrelin

A

drive the anticipation of food and hunger

38
Q

action of ghrelin

A

Stimulates NPY/Agrp neurons.
Inhibits POMC neurons.
Increases appetite - and food intake

39
Q

affect of adding Ghelin to rats

A

Fool body to think it is fasting – make think nutritional state is different

40
Q

gut hormones as a treatment of obesity

A

novel
target only relevant circuits
released daily - no side effects
Wouldn’t ware off because go throughout live nbormally

41
Q

GLP1 analogue

A

GLP1 suppress appetite

approved for diabetes and obesity = few Kg weight loss

42
Q

how can we tell that the obesity epidemic is not just related to genetics

A

it has happened to fast for a change in genetics

43
Q

what is responsible for the epidemic

A

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

ailmentary (15 decks)

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