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Met2 > Appetite regulation > Flashcards

Appetite regulation Flashcards

1
Q

What is the main centre for appetite regulation called and where is it?

A

Arcuate nucleus which is located in the hypothalamus

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2
Q

What are orexigenic signals? Give examples.

A
  • appetite stimulants
  • melanocrotin receptor antagonists

Examples:

  • agouti related peptide
  • NPY neurone
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3
Q

What are anorexigenic signals? Give examples.

A
  • melanocortin receptor agonists
  • appetite inhibiting

Examples:

  • proopiomelanocortin (POMC)
  • cocaine and amphetamine regulated transcript (CART)
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4
Q

How is satiety stimulated by chemoreceptors in the GIT?

A
  • nutrients activate receptors on enteroendocrine cells
  • these cells release signalling molecules
  • this stimulates vagal afferents which mediate the response to the brain
  • stimulate anorexigenic signals and inhibits orexigenic signals
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5
Q

How is satiety stimulated by mechanoreceptors?

A
  • distension of the GIT stretches the mechanoreceptors

- sends signals along the vagus nerve and stimulates anorexigenic signals and inhibits orexigenic signals

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6
Q

Give examples of hormones/peptides that are anorexigenics?

A
  • leptin
  • CCK
  • PYY3-36
  • insulin
  • GLP-1
  • oxyntomodulin
  • POMC
  • CART
  • melanocyte-simulating hormones
  • serotonin
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7
Q

Give examples of hormones/peptides that are orexigenics?

A
  • ghrelin
  • orexin
  • neuropeptide Y
  • AgRP
  • melanin-concentrating hormone
  • galanin
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8
Q

Leptin:

  • what is its pattern of secretion?
  • what is its effect on hunger and satiety centres?
  • when can leptin be used as a treatment?
A
  • what is its pattern of secretion? Diurnal (active during day/inactive at night)
  • what is its effect on hunger and satiety centres?
    1. inhibits NPY/AgRP
    2. activates POMC/CART
  • when can leptin be used as a treatment? give leptin injections in congenital leptin deficiency in children
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9
Q

Cholecystokinin:

  • where is it synthesised?
  • what is its effect on hunger and satiety?
A
  • where is it synthesised? duodenum (released in response to fat and protein)
  • what is its effect on hungry and satiety? slows gastric emptying, releases bile and pancreatic enzymes
  • -> helps promote feelings of satiety via activation of vagus n
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10
Q

Pancreatic peptide Y 3-36:

  • where is it released?
  • what stimulates its release?
  • what is its effect on hunger and satiety centres?
A
  • where is it released? L cells (type fo ECC)
  • what stimulates its release? high fat/protein
  • what is its effect on hunger and satiety centres? inhibits NPY and activates POMC
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11
Q

Insulin?

- what is its effect on hunger and satiety centres?

A
  • inhibit NPY/AgRP

- activate alpha MSH/CART

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12
Q

How does GLP-1 regulate appetite?

A
  • released in response to food intake

- reduced blood glucose and therefore reduces food intake

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13
Q

How does oxyntomodulin regulate appetite?

A

reduces ghrelin levels in plasma which may increase energy expenditure and increase weight loss
(suppresses appetite)

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14
Q

How does Ghrelin affect appetite?

A
  • stimulates NPY and AgRP

- acts directly on the hypothalamus via the vagus

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15
Q

Where is ghrelin synthesised?

A
  • fundus of the stomach
  • duodenum
  • ileum
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16
Q

What does chronic administration of ghrelin result in?

A

hyperphagia

17
Q

What role does the ventromedial nucleus of the hypothalamus play in appetite?

A

Promotes satiety

18
Q

What receptor is activated by NPY? What is the effect of this?

A

Y1 receptors
Effect:
- increased food intake (by activating 2nd order neurones)
- inhibits POMC/CART

19
Q

What receptor is antagonised by AgRP?

A

Melanocortin receptor

20
Q

What can be the result of POMC deficiency?

A

Hyperphagia and obesity

21
Q

What is the effect of activation of POMC/CART?

A

Reduced food intake via release of melanocortins

22
Q

What is the effect of melanocortin release?

A

alpha-melanocyte-stimulating hormone

  • activates 2nd order neurones (MCR4 receptors)
  • inhibits NPY/AgRP (MCR3 receptors)
23
Q

How does malonyl CoA regulate appetite?

A
  • inhibits lipolysis (carnitine shuttle) at high levels
  • lipolysis is stimulated at low levels
  • malonyl CoA increases in the cytoplasm (for FA synthesis) –> sensed by hypothalamus
  • suppresses AgRP and NPY
  • decreases appetite
  • malonyl CoA reduces in cytoplasm (no FA synthesis)
  • sensed by hypothalamus
  • activates AgRP and NPY
24
Q

What effect does serotonin have on appetite?

A
  • augmentation of brain 5-HT inhibits food intake + depletion of 5-HT promotes weight gain
  • serotonin increases signalling in POMC (via 5HT2cR)
  • decreases signalling in AgRP (via 5HT1bR)
25
Q

How can cannabinoids be used as drug treatments in relation to hunger/satiety?

A
  • cannabinoids increase food intake
  • THC and CBD are exogenous; anandamide and 2-arachadonylglycerol are endogenous
  • high expression of CB1 receptors in the hypothalamus

Met2 (26 decks)

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