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LCRS Endo > Endocrine control of food intake > Flashcards

Endocrine control of food intake Flashcards

1
Q

what allows the brain to access peripheral hormones?

A

the incomplete brain barrier located at the arcuate nucleus location (cricumventricular organ)

arcuate nucleus is at the hypothalamus
solitary nucleus is in the medulla (below)

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2
Q

what integrates central and peripheral feeding signals?

A

arcuate nucleus

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3
Q

what are the two main neuronal populations?

A

stimulatory- increase appetite (NPY/Agrp)

inhibitory- decrease appetite (POMC)

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4
Q

what are the stimulatory neurones of the arcuate nucleus?

where do these neurone goes

A

NPY/Agrp

goes to the lateral hypothalamus

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5
Q

what are the inhibitory neurones of the arcuate nucleus and where do they go?

A

POMC

goes to the ventromedial nucleus

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6
Q

where do there arcuate nucleus neurones travel

A

the arcuate itself is in the hypothalamus
the neurones extend to other hypothalamic regions (lateral hypothalamus and ventromedial nucleus) and extra-hypothalamic regions

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7
Q

which nucleus do BOTH Agrp/NPY and POMC neurone axons extend to?

what does this nucleus contain?

A

paraventricular nucleus

MC4R

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8
Q

what is the effect of Agrp neurone on MC4R (Melanocortin 4 receptor)?

A

Agrp (an appetite stimulatory) would inhibit MC4R to increase appetite

(MCR4 is the target for alpha MSH of POMC to stop feeling hungry all time i.e. is anti-hunger)

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9
Q

what is the effect of POMC neurone on MC4R

A

POMC is cleaved into alpha-MSH which stimulates MC4R to decrease appetite

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10
Q

what defects lead to morbid obesity?

what is the effect of a POMC deficiency?

A

POMC deficiency and MC4R mutations
POMC def leads to lack of cortisol

[no known NPY/Agrp mutations]

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11
Q

what does the ob/ob mouse show about the importance of leptin?

A

The effects of missing leptin:

  • recessive mutations led to obesity, diabetes, infertility and stunted growth, low immune function, decreased body temp
  • There were abnormalities comparable to a starved animals
  • The mouse eats a lot thinking it has no fat in the body
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12
Q

leptin levels according to body fat
low BF-
high BF-

A

low BF- low leptin

high BF- high leptin

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13
Q

effect of leptin administration

A

decreased food intake
increased thermogenesis

restores LH pulsatility therefore enabling normal puberty and menstrual cycles

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14
Q

why is leptin an ineffective weight control drug

A

obesity is due to leptin resistance so leptin has no efficacy on the receptor despite having high leptin

leptin is anti-starvation rather than anti-obesity

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15
Q

what is the effect of leptin on the neurones

A

activates POMC–> increase satiety

inhibits NPY/Agrp–> decrease appetite

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16
Q

what are the effects of an absence of leptin

A

o Hyperphagia, lowered energy expenditure and sterility – like effects of starvation.
- ammenorhoea

o Leptin is an anti-starvation hormone and so presence of leptin tells the brain that one has sufficient fat reserves for normal functioning (but high leptin has little effect).

17
Q

how does the circulation of insulin compare to body fat

A

proportional

18
Q

where are insulin receptors found

what is the effect of central administration of insulin

A
  • receptors in the hypothalamus

- central administration reduces food intake

19
Q

what regulates the release of gut hormones?

A

content of the gut and therefore mechanoreceptors

20
Q

what enables Ghrelin to cross the BBB?

A

28aa gastric hormone with fatty acid group attached

21
Q

what enzyme adds the fatty group to Ghrelin?

A

GOAT
Ghrelin O-Acyltransferase
–> this activates ghrelin

22
Q

what are the effects of ghrelin on hormones and appetite?

  • on neurones
  • overall effects
A

stimulates NYP/Agrp–> stimulates appetite
inhibits POMC –> decreases satiety

  • increases appetite
  • drives hunger for food just before a meal
  • therefore increased intake
  • ghrelin falls after a meal
23
Q

what do L- cells secrete?

A

the appetite reducers:
PYY
GLP-1 (from preproglucagon gene)

glucagon is also secreted by alpha cells of the pancreas

24
Q

what is the correlation between PYY and calories?

A

PYY aims to reduce appetite:

more calories in the food –>more PYY released by the L cells

25
Q

how is PYY activated?

  • process
  • enzyme involved
A

cleaved at position 1 and 2 at N-terminal

  • tyrosine 1
  • proline 2

to form PYY3-36

  • this is done by DPP4 (di-peptidyl peptidase 4)
  • DPP4 is also involved in the metabolism of GLP-1 (incretins)
26
Q

what is the effect of PYY?

A
  • inhibits NPY neurones–> decreased appetite
  • stimulates POMC –> increased satiety

overall reduced hunger
“a meal has been had”

27
Q

when is GLP-1 released?

A

post-prandial

28
Q

what is the effect of GLP-1?

A

incretin effect:

in stimulating glucose-stimulated insulin release to reduce food intake

29
Q

gut hormone summary

A

increase appetite- Ghrelin

decrease appetite- PYY, GLP-1

30
Q

saxenda

A

liraglutide

long-acting glucagon-like peptide-1 receptor agonist

reduces food intake

31
Q

what is the dosage of Saxenda/liraglutide for T2DM

A

double

GLP-1 agonists

32
Q

how is GLP-1 inhibited quickly?

A

by metabolism by:
DPP-4 (gliptins)
causes inactivation

33
Q

why is PYY3-36 a hard target for drug manipulation?

A

narrow therapeutic window

34
Q

Genetics hypotheses for obesity prevalence [2]

A

o Thrifty gene hypothesis: SURVIVAL

  • Specific genes are selected for to increase metabolic efficiency and fat storage.
  • It makes evolutional sense to put on weight.
  • Thin humans didn’t survive famines so didn’t pass genes on to modern humans.

o Drifty gene hypothesis (ADAPTIVE drift):

  • There is a normal distribution of body weight – the fat people were eaten, the thin starved.
  • However, 10k-20k years ago, humans learned to defend themselves and so obesity was not selected against so obesity was a neutral change (whilst the thin still starved).

environment only plays a role in obesity when one is genetically prone to obesity

35
Q

describe the pathway that stimulates hunger or satiety

A
  • mechanoreceptors in the stomach detect stretch
  • low stretch means increased hunger due to decreased receptor firing
  • VAGUS carries signal to SOLITARY nucleus in the medulla
  • solitary nucleus to the ARCUATE nucleus in the hypothalmaus
  • the arcuate sends orexinogenic projections to the LATERAL HYPOTHALAMUS to stimulate appetite (Agrp/NPY) nb involved in wakefulness
  • the arcuate sends anorexigenic projections to the VENTROMEDIAL nucleus to increase satiety (POMC)

LCRS Endo (18 decks)

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