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BRS Year 2 > Gastro appetite > Flashcards

Gastro appetite Flashcards

1
Q

is obesity associated with high or low income countries?

A

low

-> historically was high

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2
Q

3 triggers for thirst

A
  1. body fluid osmolality
  2. blood volume reduction
  3. blood pressure is reduced
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3
Q

what is the most potent of the 3 triggers for thrist?

A

body fluid osmolality
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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4
Q

hormone that controls osmolality

A

ADH/ vasopressin

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5
Q

where does ADH act?

A

aquaporin 2 of the collecting duct (increase of aquaporin 2 insertion on membrane), acting on the kidney

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6
Q

what happens when ADH is low?

A

large volume of urine is excreted (water dieuresis)

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7
Q

what is the term for when lots of ADH prevents excretion of large volumes of dilute urine?

A

anti-diuresis

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8
Q

where is ADH stored in the body?

A

the posterior pituitary gland

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9
Q

what receptors measure osmolality? Where are they found?

A
  • osmoreceptors

- found in the hypothalamus

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10
Q

in which regions of the hypothalamus are osmoreceptors found? (2)

A
  1. organum vasculosum of the lamina terminalis

2. subfornical organ

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11
Q

what happens to osmoreceptors when solution is hypertonic

A

Cells shrink when plasma more concentrated (lower plasma osmolality)
Proportion of cation channels increases – membrane depolarizes
Send signals to the ADH producing cells to increase ADH
Fluid retention
Invokes drinking

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12
Q

Where are receptors for thirst located?

How long does the thirst sensation last at these receptors?

A 
receptors in the:
1. mouth
2. pharynx
3. oesophagus
Relief of thirst sensation via these receptors is short lived.
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13
Q

when is thirst completely satisfied?

A

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

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14
Q

what system controls blood pressure/volume

A

renin-angiotensin-aldosterone system

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15
Q

which cells are activated by low BP?

A

juxtaglomerular cells of renal afferent arterioles: leads to production of renin

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16
Q

what does renin release cause?

A

production of angiotensin I (renin is an enzyme that cleaves angiotensinogen to form angiotensin I)

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17
Q

what is angiotensin I converted into in the blood?

A

angiotensin II

-> facilitated by ACE in the lungs

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18
Q

what does angiotensin II promote?

A
  • vasoconstriction - increase sympathetic activity
  • thirst
  • ADH secretion
  • Aldosterone release (from zona glomerulosa)
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19
Q

what does aldosterone do in the renin-angiotensin-aldosterone system?

A

H2O retention via Na+Cl- absorption and K+ excretion

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20
Q

which structure is most important in regulating appetite?

A

the hypothalamus

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21
Q

hormones that regulate appetite?

A

GHRELIN
PYY
LEPTIN

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22
Q

other than hormones, what can influence how the hypothalamus regulates appetite?

A

neural input from the periphery and other brain regions via vagus

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23
Q

what does orexigenic mean?

A

appetite stimulant

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24
Q

what does anorectic/anorexigenic mean?

A

appetite suppresive

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25
Q

structures of the hypothalamus (4)

A
  1. arcuate nucleus
  2. ventromedial hypo
  3. lateral hypo
  4. paraventricular nucleus
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26
Q

where do the orexigenic/anorectic neurons of the arcuate nucleus feedback to in the hypothalamus?
What is this structures role?

A

the paraventricular nucleus

Fibres project to posterior pituitary (release of oxytocin and ADH)

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27
Q

how does the arcuate nucleus control appetite?

A

through orexigenic and anorectic neurons

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28
Q

Where does the paraventricular nucleus project to?

A

Posterior pituitary where in releases ADH and oxytocin

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29
Q

what is the ventromedial hypothalamus associated with?

A

satiety -> lesions in the this region in rats leads to severe obesity

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30
Q

What does POMC (pro-opiomelanocortin) do to the arcuate nucleus?

A

activates it = lower food intake

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31
Q

What does the lateral hypothalamus produce?

A

only orexigenic peptides

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32
Q

examples of chemicals that affect appetite?

A

endocannabinoids, AMPK, tyrosine phosphatase

33
Q

what does the arcuate nucleus produce?

A

peptides: orexigenic peptides and anorectic peptides

34
Q

What feature of the arcuate nucleus means that it is able to access peripheral hormones

A

Incomplete blood brain barrier

35
Q

What does the arcuate nucleus integrate

A

peripheral and central feeding signals

36
Q

what are the two neuronal populations of the arcuate nucleus?

A

stimulatory (NPY/AGRP)

inhibitory (POMC)

37
Q

What does leptin stimulate in the arcuate nucleus?

What is its effect?

A

POMC/CART neurons

High leptin stimulates these neurons to decrease feeding and produce satiety

38
Q

NPY/Agrp neuron have receptors for what hormones?
What is their action?
When are they activated?

A

leptin and insulin
Leptin inhibits NPY/AGRP
Inc. NPY/AGRP signalling stimulates food intake
->activated when leptin is decreased e.g. when fasting, have uncontrolled diabetes or genetic leptin deficiency

39
Q

what systems other than GI is the arcuate nucleus involved in?

A

fertility and cardiovascular regulations

40
Q

When POMC is stimulated, what is created?

A

production of a-MSH (a melanocortin)

This leads to production of MC4R

41
Q

what are MC4-receptors stimulated by?

What is their action?

A

serotonin to reduce appetite and food intake

42
Q

are any NPY or Agrp mutations associated with appetite in humans?

A

none discovered

43
Q

deficiency in what can cause morbid obesity?

A

POMC

44
Q

mutation to what receptor can cause morbid obesity?

A

MC4-R

45
Q

why is the amygdala important for appetite

A

involved in emotion, memory -> reward pathways

-> contributes to appetite

46
Q

what does the lateral hypothalamus produce that affects appetite?

A

appetite stimulants

47
Q

What does the adipostat mechanism do?

A

keep fat mass within a narrow range

48
Q

What is the adipostat mechanism?

A

Circulating hormone produced by fat

Hypothalamus senses the concentration of hormone.

Hypothalamus then alters neuropeptides to increase or decrease food intake.

Perhaps a problem with the regulation of the adipostat mechanism leads to obesity ?

49
Q

how many neural pathways are associated with the adipostat mechanism?

A

2 hypothalamic neural pathways

50
Q

where is leptin made?

A

by adipocytes in white adipose tissue + enterocytes

51
Q

How does leptin travel?

A

in the body plasma

52
Q

where does leptin act in the hypothalamus?

What is its effect?

A

the arcuate nucleus

Regulates appetite and thermogenesis (expenditure)

53
Q

What are high levels of leptin associated with?

A

Atherosclerosis development via innate system

54
Q

What conditions are low levels of leptin associated with?

A

depression

Alzheimer’s

55
Q

features of congenital leptin deficiency

A

normal birth weight
excessive eating = early childhood obesity
Rare

56
Q

How is body fat associated with serum leptin?

A

Inc. serum leptin in obese subjects suggests obese subjects become insensitive to leptin

57
Q

3 ways which leptin can fail:

A
  1. insufficient production -> deficiency
  2. leptin resistance -> like T2DM: inability to detect satiety despite high energy store
  3. regulatory defect -> low leptin despite high BMI
58
Q

WHat can leptin resistance lead to?

A

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

59
Q

Why do we feel less hungry after meal?

  1. bulk in tum
  2. nutrients in circulation
  3. Hormones from gut
A

hormones in gut (3)

60
Q

2 GI hormones that control appetite and their actions?

A

Ghrelin
Stimulates appetite, increases gastric emptying

Peptide YY
Inhibits food intake

61
Q

what secretes the GI hormones?

A

enteroendocrine cells in the stomach, pancreas and SB

62
Q

what do GI hormones do?

A

control various functions of digestive organs (motility, appetite, satiety)

63
Q

When are blood levels of ghrelin highest? What happens?

A

before meals

  • > help prepare for food intake by inc gastric motility and acid secretion
  • > increases appetite
64
Q

which nucleus does ghrelin directly modulate?

A

the arcuate nucleus

  • > stimulates NPY/Agrp neurons
  • > inhibits POMC
65
Q

what does ghrelin regulate

A

-> involved in regulation of reward, taste sensation, memory and circadian rhythm

66
Q

what type of rhythm does ghrelin have?

A

diurnal- this plays a role in meal regulation

67
Q

How has ghrelin been proven to increase food intake?

A

In rats: rats given ghrelin for 7 days - cumulative inc in food intake
In humans: subjects given iV ghrelin or IV saline and given all you can eat buffet. Inc. energy consumption in subjects given ghrelin

68
Q

what does PYY stand for?

A

peptide tyrosine tyrosine

69
Q

where and when is PYY released?

A

from the terminal ileum and colon in response to feeding

70
Q

what types of food induce best PYY response

A

wholegrain food, fish proteins + fibre

71
Q

what does PYY do to appetite?

A

reduces it

-> can be digested or injected IV

72
Q

whatt does PYY release inhibit release of?

A

NPY

73
Q

which neurons are stimulated by PYY?

A

POMC

74
Q

what can PYY cause at higher dose?

A

nausea and fullness

-> food intake reduction is dose dependent

75
Q

examples of comorbidities obesity is associated with?

A 
Depression- 1/3 of patients with BMI over 30
Sleep apnoea- narrowing of trachea
Bowel cancer- proven**
Osteoarthritis
Gout
PVD
Diabetes
Hypertension
MI
Stroke
76
Q

How does environment and genetic susceptibility to obesity affect BMI?

A

not being genetically susceptible and in healthy environment has little impact on BMI
Being genetically prone and in a toxic environment increases BMI significantly

77
Q

what is the difference in how you observe leptin vs PYY satiety?

A 
leptin = longer term
PYY = immediate
78
Q

Describe weight homeostasis

A 
Weight augmented (overfed):
-Inc. sympathetic nervous system activity
-Inc. energy expenditure
-Dec. hunger/food intake
-Weight loss
Weight reduced (underfed state)
-Dec. sympathetic nervous system activity
-Dec. energy expenditure
-Inc. hunger/food intake
-Weight gain
79
Q

How does leptin levels change with body fat?

How has this been scientifically proven?

A

Low with low body fat
High with high body fat
Replacement of leptin in ob/ob mouse decreases weight

BRS Year 2 (110 decks)

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