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Sophie - Applied Physiology & Pharmacology Year 2 > 56.2 Control of Appetite > Flashcards

56.2 Control of Appetite Flashcards

1
Q

What is the satiety centre?

A

Ventromedial hypothalamic nucleus

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2
Q

What is the hunger centre?

A

Lateral hypothalamic nuclei

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3
Q

Which hypothalamic nucleus is the integrative centre for peripheral signals of appetite?

A

Arcuate nucleus

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4
Q

What are the alimentary tract hormones involved in appetite?

A

Ghrelin, insulin

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5
Q

Where and when is Ghrelin produced?

A

*Specialised endocrine P/D1 cells in gastric mucosa of stomach
*The concentration increases before a meal and drops on eating.

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6
Q

Which neurons does ghrelin stimulate?

A

NPY/AgRP neurons

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7
Q

What is the function of ghrelin?

A

ghrelin is the only gastric hormone to increase appetite and decrease metabolism

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8
Q

How do the levels of leptin and insulin change throughout the day and in contrast with each other?

A
  • Leptin levels do not change much with meals or fasting (intermediate- to long-term signal)
  • But insulin levels change dramatically in response to meals (short-term signal)
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9
Q

Where is insulin released from and when?

A

Pancreatic beta cells
After a meal in response to increased plasma glucose

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10
Q

Which neurons do leptin and insulin stimulate and inhibit?

A

Stimulate POMC/CART neurons
Inhibit NPY/AgRP neurons

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11
Q

What kind of signal does insulin have on the hypothalamus?

A

Anorexigenic

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12
Q

What is CCK?

A

Cholecystokinin

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13
Q

How does CCK signal to the brain?

A
  • Binds to receptors on vagal afferent nerves in submucosa
  • Vagal afferent signals travel to the NTS in the dorsal vagal complex
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14
Q

What stimulates CCK release?

A

A meal
- due to introduction of HCl, amino acids, or fatty acids into duodenum

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15
Q

Where is cholecystokinin (CCK) released from?

A

I-cells of the duodenum (small intestine)

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16
Q

What is PYY?

A

Peptide tyrosin tyrosin

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17
Q

What kind of signal does PYY have on the hypothalamus/NTS?

A

Anorexigenic

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18
Q

Where does PYY bind?

A

Arcuate nucleus (POMC/CART) and NTS (nucleus of the solitary tract) in brainstem

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19
Q

Where is peptide tyrosin tyrosin (PYY) released from and when?

A

Ileum and colon (distal gut)
In response to food intake (mainly fat)

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20
Q

What is PP?

A

Pancreatic polypeptide

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21
Q

What kind of signal does PP have on the brain?

A

Anorexigenic

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22
Q

Where does PP bind to?

A

Arcuate nucleus (POMC/CART) and PVN
NTS in brainstem
May also act via vagus nerve

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23
Q

Where is pancreatic polypeptide (PP) released from and when?

A

Pancreatic PP cells in islets of Langerhans
In response to a meal, in proportion to caloric intake

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24
Q

What are the effects of GLP-1?

A

Inhibits gastric emptying, promotes satiety

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25
Q

What is GLP-1?

A

glucagon-like-peptide-1

26
Q

Where does GLP-1 bind to?

A

Arcuate nucleus (POMC/CART)
NTS
Vagal afferents

27
Q

Where is glucagon-like peptide 1 (GLP-1) released from and when?

A

L-cells of the intestines
After meal ingestion

28
Q

What is Leptin?

A

peptide hormone that regulates food intake/ body mass/ reproductive function/ foetal growth/ proinflammatory immune response/ angiogenesis/ lipolysis.

29
Q

What is the effect of Leptin on the arcuate nucleus?

A
30
Q

Where is leptin synthesised and secreted from?

A

Synthesised + secreted by WAT fat cells
When lipid storage (body fat mass) increases

31
Q

What kind of signal does leptin have on the hypothalamus?

A

Anorexigenic

32
Q

What kind of signal does leptin have on the NTS?

A

Anorexigenic (satiety)

33
Q

What can leptin and leptin receptor deficiency cause?

A

It is a rare cause of major obesity

34
Q

What is congenital leptin deficiency associated with?

A

Congenital leptin deficiency is associated with severe early-onset obesity in humans

35
Q

What is the role of leptin and when is it secreted?

A
  • Leptin leads to decreased appetite
  • Leptin production increases exponentially with body fat mass, so it acts as direct feedback, maintaining weight within a narrow range
  • However, leptin levels can also be dissociated from this relationship by various events, such as starvation
36
Q

What are the central signals?

A

Neuropeptide Y (NPY), alphaMelanocyte Stimulating Hormone (alphaMSH), mesolimbic reward system, social cues.

37
Q

How do POMC/CART and NPY/AgRP neurons interact?

A

NPY/AgRP have an inhibitory effect on POMC/CART neurons through GABA release

38
Q

How is the orbitofrontal cortex involved in food intake?

A

Part of integrating sensory inputs to make decisions
Combines info about taste, smell, visual inputs, texture
Directs which foods to avoid and which to seek out

39
Q

How is the VTA involved in food intake?

A
  • After eating, signals rewards
  • Leptin receptors activated (full) - decreases dopamine release, increases dopamine reuptake
  • Ghrelin receptors activated (hungry) - increases dopamine release
    Explains why food ‘tastes better’ when you are more hungry
40
Q

What are the downstream effects of stimulation of MC4Rs?

A
  • Promotes satiety and decreases food intake via stimulation of lateral parabrachial nucleus
  • Increases energy expenditure via activation of descending sympathetic pathways
41
Q

What are the functions of the NPY/AgRP and POMC/CART neurons?

A

NPY/AgRP: orexogenic, signalling hunger
POMC/CART: anorexigenic, signalling satiety

42
Q

What are the second-order neurons that POMC/CART and NPY/AgRP neurons project to called?

A

PVN satiety neurons/PVN anorexogenic centres

43
Q

What are the two main opposing types of neurons in the arcuate nucleus?

A

NPY/AgRP
POMC/CART

44
Q

What can abnormalities in rewarding eating behaviours lead to?

A

Eating disorders

Reward perverted towards low energy dense foods despite starvation, implicit ‘wanting’ of low cal foods

45
Q

What does anorexigenic mean?

A

Reduces appetite
(/stimulates satiety)

46
Q

What does destruction of the lateral nucleus lead to?

A

Anorexia

47
Q

What does destruction of the ventromedial nucleus lead to?

A

Hyperphagia

48
Q

What does orexigenic mean?

A

Stimulates appetite
(/inhibits satiety)

49
Q

What is the mechanism of action of AgRP?

A

Inverse agonist at MC4Rs - inhibits the satiety response brought about by MC4R activation

50
Q

What is the mechanism of action of GABA?

A

Inhibitory neurotransmitter at GABA-A and GABA-B
Allows NPY/AgRP neurons to inhibit POMC/CART neurons
Inhibits activation of lateral parabrachial nucleus

51
Q

What is the mechanism of action of NPY?

A

Agonist at Y receptors
Potent orexigenic peptide - induces a robust feeding response

52
Q

What is the role of the nucleus accumbens in food reward?

A
  • Gives feeling of pleasure/reward
  • Elicits neuronal activation for foods that were previously stimulatory: i.e. the reinforcing value of food
  • Links flavours paired with more calories with greater reward
53
Q

Where do neurons from the VTA project to?

A

Nucleus accumbens

54
Q

Where do the POMC/CART and NPY/AgRP neurons in the arcuate nucleus project to?

A

Paraventricular nucleus (PVN)

55
Q

Where is the hub of the mesolimbic reward system?

A

Ventral tegmental area (VTA)

56
Q

Which hormone is chronically increased in Prader-Willi syndrome?

A

Ghrelin
Constant orexigenic signalling –> hyperphagia

57
Q

Which neurotransmitter do POMC/CART neurons release?

A

α-melanocyte stimulating hormone (α-MSH)

58
Q

Which neurotransmitters do NPY/AgRP neurons release?

A
  • Neuropeptide NPY
  • AgRP
  • GABA
59
Q

Which receptor does α-MSH bind to?

A

Melanocortin 4 (MC4) receptor

60
Q

Which top-down factors can affect food intake?

A

Social cues, emotional cues, hedonistic behaviours

Sophie - Applied Physiology & Pharmacology Year 2 (32 decks)

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