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Z YEAR 2 BRS GASTRO > Appetite > Flashcards

Appetite Flashcards

1
Q

What controls thirst?

A
  1. Body fluid osmolality
  2. Blood volume is reduced
  3. Blood pressure is reduced
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2
Q

What is the most potent stimulus for thirst?

A
  • Plasma osmolality increase is the more potent stimulus – change of 2-3% induces strong desire to drink
  • Decrease of 10-15% in blood volume or arterial pressure is required to produce the same response
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3
Q

How is osmolarity controlled?

A

ADH/vasopressin

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4
Q

Where does ADH work?

A
  • Acts on the kidneys to regulate the volume and osmolality of urine
  • Collecting duct - Aquaporin 2 channel
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5
Q

What happens when plasma ADH is low?

A

large volume of urine is excreted (water diuresis)

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6
Q

What happens when plasma ADH is high?

A

small volume of urine is excreted (anti diuresis)

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7
Q

What are osmoreceptors?

A
  • Sensory receptors
  • Osmoregulation
  • Found in the hypothalamus
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8
Q

Which regions are these osmoreceptors found in the hypothalamus?

A
  • Organum vasculosum of the lamina terminalis (OVLT)

* Subfornical Organ (SFO)

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9
Q

How do osmoreceptors control ADH release?

A
  1. Cells shrink when plasma more concentrated
  2. Proportion of cation channels increases – membrane depolarizes
  3. Send signals to the ADH producing cells to increase ADH
  4. Fluid retention, Invokes drinking
    - And vice versa
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10
Q

When is thirst decreased?

A

by drinking even before sufficient water has been absorbed by the GI tract to correct plasma osmolality

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11
Q

Where are receptors for sensation of thirst?

A
  • mouth, pharynx, oesophagus are involved

- Relief of thirst sensation via these receptors is short lived

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12
Q

When is thirst completely satisfied?

A

once plasma osmolality is decreased or blood volume or arterial pressure corrected

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13
Q

What happens when BP decreases?

A
  1. Juxtaglomerular cells of renal afferent arteriole

2. Angiotesinogen (renin) convert angiotensin I in liver

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14
Q

What does angiotensin II control?

A
  1. Thirst
  2. Vasoconstriction, increase sympathetic activity
  3. H2O retnetion via Na+Cl- absorption and K+ excretion
  4. ADH secretion
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15
Q

What does a reduction in fat mass increase?

A

food intake and reduces energy expenditure

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16
Q

What does adipose tissue expansion reduce?

A

food intake and increases energy expenditure

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17
Q

What happens in a weight reduced - underweight state?

A
  1. Decrease sympathetic nervous activity
  2. Decrease energy expenditure
  3. Increase hunger/food intake
  4. Decrease thyroid
    - Weight regain
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18
Q

What happens in a weight augmented - overfed state?

A
  1. Increase in sympathetic nervous system activity
  2. Increase energy expenditure
  3. Decrease hunger/food. intake
    - weight loss
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19
Q

What inputs to the hypothalamus for appetite regulation?

A
  1. GHRELIN, PYY & other gut hormones
  2. Neural input from the periphery and other brain regions
  3. Leptin
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20
Q

What does the hypothalamus deliver in appetite regulation?

A
  1. Food intake

2. Energy expenditure

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21
Q

What parts of the hypothalamus is involved in appetite?

A
  1. Paraventricular nucleus
  2. Lateral hypothalamus
  3. Ventromedial hypothalamus
  4. Arcuate nucelus (medial basal part) - productive orexigenic, and anirexigenic appeitie
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22
Q

What is the arcuate nucleus?

A

Brain area involved in the regulation of food intake

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23
Q

What is the BBB for the arcuate nucleus?

A

Incomplete blood brain barrier, allows access to peripheral hormones.

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24
Q

What does the arcuate nucleus integrate?

A

peripheral and central feeding signals

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25
Q

What are the two neuronal population in the arcuate nucleus?

A
  • Stimulatory (NPY/Agrp neuron)

* Inhibitory (POMC neuron)

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26
Q

What mutations are not involved in appetite?

A

No NPY or Agrp mutations associated with appetite discovered in humans

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27
Q

What mutations cause morbid obesity?

A
  • POMC deficiency
  • MC4-R mutations
  • Mutations not responsible for the prevalence of obesity - but useful to explain signaling
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28
Q

What signals from other brain regions are involved in appetite?

A
  1. Higher centres
  2. Amygdala- emotion, memory
  3. Other parts of the hypothalamus, e.g. lateral hypothalamus
  4. Vagus to brain stem to hypothalamus
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29
Q

What is adipostat?

A

Circulating hormone produced by fat

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30
Q

How does the hypothalamus deal with adipostat mechanism?

A
  1. Hypothalamus senses the concentration of hormone.
  2. Hypothalamus then alters neuropeptides to increase or decrease food intake.
  3. Perhaps a problem with the regulation of the adipostat mechanism leads to obesity ?
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31
Q

Where is leptin made?

A

by adipocytes in white adipose tissue

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32
Q

How does leptin circulate?

A

in plasma

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33
Q

What does leptin act on?

A

upon the hypothalamus regulating appetite (intake) and thermogenesis (expenditure)

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34
Q

What is congenital leptin deficiency?

A
  • In these children leptin has been effective in reducing body weight.
  • Only few people known to have this defect
35
Q

What is the mechanism of leptin?

A
  1. Decreased leptin expression / secretion in adipose
36
Q

When is leptin low?

A

when low body fat

37
Q

When is leptin high?

A

when high body fat

38
Q

What does leptin do?

A
  • Hormone that decreases food intake and increases thermogenesis
  • Replacement in the ob/ob mouse decreases weight
39
Q

What is the concentration of leptin circulating in the plasma proportional to?

A

fat mass

40
Q

When is there high leptin?

A

fat person

41
Q

Is leptin effective as a weight control drug?

A

no

42
Q

When is obesity due to?

A

Obesity due to leptin resistance- hormone is present but doesn’t signal effectively

43
Q

Why do we feel less hungry after a meal?

A

Hormonal Signal from the gut

44
Q

What are gastrointestinal hormones secreted by?

A
  • Secreted byenteroendocrine cellsin thestomach, pancreas & SB
  • Control various function of digestive organs
45
Q

Which hormones regulate appetite?

A
  1. Ghrelin

2. Peptid YY

46
Q

What is cholecystokinin used for?

A
  1. Gallbladder contraction
  2. Gastrointestinal motility
  3. Pancreatic exocrine secretion
47
Q

What is secretin used for?

A

Pancreatic exocrine secretion

48
Q

What is GIP used for?

A

Incretin activity

49
Q

What is motilin used for?

A

Gastrointestinal motility

50
Q

What is ghrelin used for?

A
  1. Hunger

2. Growth hormone release

51
Q

What is gastrin used for?

A

Acid secretion

52
Q

What is insulin and glucagon used for?

A

Glucose homeostasis

53
Q

What is pancreatic polypeptide used for?

A
  1. Gastric motlity

2. Satiation

54
Q

What is amylin used for?

A
  1. Glucose homestasis

2. Gastric motility

55
Q

What is GLP-1 used for?

A
  1. Incretin activity

2. Satiation

56
Q

What is GLP-2 used for?

A

Gastrointestinal motility and growth

57
Q

What is oxyntomodulin used for?

A
  1. Satiation

2. Acid secretion

58
Q

What is PYY3-36 used for?

A

Satiation

59
Q

What does ghrelin do?

A
  • Stimulates appetite

- Increases gastric emptying

60
Q

What does peptide YY do?

A

Inhibits food intake

61
Q

When are blood levels of ghrelin highest and why?

A
  • before meals

- help prepare for food intake by increasing gastric motility and acid secretion

62
Q

How does ghrelin directly modulate neurons in the arcuate nucelus?

A
  • Stimulates NPY/Agrp neurons.

* Inhibits POMC neurons.

63
Q

What else does ghrelin do?

A
  • Increases appetite

* Regulation of reward, taste sensation, memory, circadian rhythm

64
Q

When is peptide tyrosine tyrosine (PYY) released?

A
  • in the terminal ileum (TI) and colon in response to feeding (36 Amino acids)
  • Food arriving to the TI and colon results in PYY release
65
Q

What does PYY do?

A
  1. Reduces appetite – can be digested or injected IV
  2. Inhibits NPY release
  3. Stimulates POMC neurons
66
Q

What happens to angiotensiin I in lungs?

A

converted to angiotensin II by ACE

67
Q

What does angiotensin do with aldosterone?

A
  1. Binds to receptors on intraglomerular messenger cells
  2. Causes cell to contract along with the blood vessels surrounding them
  3. Leads to release of aldosterone in zona glomerulosa of the adrenal cortex
  4. Aldosteorne role in sodium conservation
    - H2O retention via Na+Cl- absoprtion and K+ excretion
    - Aldosterone in BP
68
Q

What are ACE/renin inhibitors used for?

A

treat high BP

69
Q

What is the arcuate nucleus?

A

(aggregation of neurons in medial basal part) - adjacent to third ventricle and produces orexigenic and anirexigenic appetite

70
Q

What are the terminal fields of these neurons?

A

is the paraventricular nucleus (adjacent to 3rd ventricle) and contains neurons that project to the posterior pituitary

71
Q

What do these projecting neurons secrete?

A

oxytocin and ADH (affects osmoregulation, appetite and stress reaction of the body)

72
Q

What does the lateral hypothalamus produce?

A

only produces orexigenic peptides

73
Q

What is the ventromedial hypothalamus associated with?

A

satiey and lesions in this region in rats leads to severe obesity

74
Q

What do melanocortins in the ventormedial hypothalamus regulate?

A

feeding behaviour

75
Q

When does food intake decrease?

A

when the arcuate nucleus POMC neurons activate

76
Q

What are other hypothalamic factors recently implicated in appetite regulations?

A
  • endcannabinoids
  • AMP
  • protein tyrosine phosphatase
77
Q

Where are NPY/Agrp neurons found?

A

only found in hypothalamic arcuate nucleus

78
Q

What do NPY/Agrp neurons do?

A
  1. make peptides that potentially stimulate food intake by increasing neuropeptide Y signalling and reducing melanocortin signalling via the release of AGRP, an endogenous melanocortin receptor antagonist
  2. These neurons also express receptors for leptin and insulin, as they are activated by a decrease of leptin or insulin signalling
  3. Fasting, uncontrolled diabetes and genetic leptin deficiency are examples of conditions in which food intake increases by this mechanism
79
Q

What happens when circulating factors reach POMC/NPY/Agrp?

A
  1. activate POMC which then decreases feeding

2. can activate NPY/AGRP neurons which then increases feeing both of these go through the third ventricle nucleus

80
Q

Besides feeding what else is the arcuate nucleus involved in?

A

fertility and cardiovascular regulation

81
Q

What are melanocortins?

A

products of POMC e.g.alpha MSH

82
Q

What is the melanocortin system?

A
  1. central regulator of energy balance, in both feeding behaviours and energy expenditure
  2. Melanocortin-4 receptors expressed in paraventricular nucleus
  3. These receptors are stimulated by serotonin and they lead which leads to reduction of appetite and weight and decreased food intake
83
Q

What are serum leptin levels in obese?

A

serum leptin significantly higher in obese people and and serum leptin concentrations are correlated with the percentage of body fat suggesting that most obese people are insensitive to endogenous leptin production

84
Q

What can affect the leptin mechanism?

A
  1. Insufficient production of leptin
  2. Receptor signalling or the regulatory signalling can be defective and reduce leptin levels despite high adipose tissue mass can occur
  3. Could also be a decreases sensitivity to leptin (similar to insulin deficiency in T2 diabetes) which results in inability to detect satiety despite high energy stores and high levels
    look at data1

Z YEAR 2 BRS GASTRO (15 decks)

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