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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
structures of the hypothalamus (4)
1. arcuate nucleus 2. ventromedial hypo 3. lateral hypo 4. paraventricular nucleus
26
where do the orexigenic/anorectic neurons of the arcuate nucleus feedback to in the hypothalamus? What is this structures role?
the paraventricular nucleus | Fibres project to posterior pituitary (release of oxytocin and ADH)
27
how does the arcuate nucleus control appetite?
through orexigenic and anorectic neurons
28
Where does the paraventricular nucleus project to?
Posterior pituitary where in releases ADH and oxytocin
29
what is the ventromedial hypothalamus associated with?
satiety -> lesions in the this region in rats leads to severe obesity
30
What does POMC (pro-opiomelanocortin) do to the arcuate nucleus?
activates it = lower food intake
31
What does the lateral hypothalamus produce?
only orexigenic peptides
32
examples of chemicals that affect appetite?
endocannabinoids, AMPK, tyrosine phosphatase
33
what does the arcuate nucleus produce?
peptides: orexigenic peptides and anorectic peptides
34
What feature of the arcuate nucleus means that it is able to access peripheral hormones
Incomplete blood brain barrier
35
What does the arcuate nucleus integrate
peripheral and central feeding signals
36
what are the two neuronal populations of the arcuate nucleus?
stimulatory (NPY/AGRP) | inhibitory (POMC)
37
What does leptin stimulate in the arcuate nucleus? | What is its effect?
POMC/CART neurons | High leptin stimulates these neurons to decrease feeding and produce satiety
38
NPY/Agrp neuron have receptors for what hormones? What is their action? When are they activated?
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
what systems other than GI is the arcuate nucleus involved in?
fertility and cardiovascular regulations
40
When POMC is stimulated, what is created?
production of a-MSH (a melanocortin) | This leads to production of MC4R
41
what are MC4-receptors stimulated by? | What is their action?
serotonin to reduce appetite and food intake
42
are any NPY or Agrp mutations associated with appetite in humans?
none discovered
43
deficiency in what can cause morbid obesity?
POMC
44
mutation to what receptor can cause morbid obesity?
MC4-R
45
why is the amygdala important for appetite
involved in emotion, memory -> reward pathways | -> contributes to appetite
46
what does the lateral hypothalamus produce that affects appetite?
appetite stimulants
47
What does the adipostat mechanism do?
keep fat mass within a narrow range
48
What is the adipostat mechanism?
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
how many neural pathways are associated with the adipostat mechanism?
2 hypothalamic neural pathways
50
where is leptin made?
by adipocytes in white adipose tissue + enterocytes
51
How does leptin travel?
in the body plasma
52
where does leptin act in the hypothalamus? | What is its effect?
the arcuate nucleus | Regulates appetite and thermogenesis (expenditure)
53
What are high levels of leptin associated with?
Atherosclerosis development via innate system
54
What conditions are low levels of leptin associated with?
depression | Alzheimer's
55
features of congenital leptin deficiency
normal birth weight excessive eating = early childhood obesity Rare
56
How is body fat associated with serum leptin?
Inc. serum leptin in obese subjects suggests obese subjects become insensitive to leptin
57
3 ways which leptin can fail:
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
WHat can leptin resistance lead to?
Obesity due to leptin resistance- hormone is present but doesn’t signal effectively
59
Why do we feel less hungry after meal? 1. bulk in tum 2. nutrients in circulation 3. Hormones from gut
hormones in gut (3)
60
2 GI hormones that control appetite and their actions?
Ghrelin Stimulates appetite, increases gastric emptying Peptide YY Inhibits food intake
61
what secretes the GI hormones?
enteroendocrine cells in the stomach, pancreas and SB
62
what do GI hormones do?
control various functions of digestive organs (motility, appetite, satiety)
63
When are blood levels of ghrelin highest? What happens?
before meals - > help prepare for food intake by inc gastric motility and acid secretion - > increases appetite
64
which nucleus does ghrelin directly modulate?
the arcuate nucleus - > stimulates NPY/Agrp neurons - > inhibits POMC
65
what does ghrelin regulate
-> involved in regulation of reward, taste sensation, memory and circadian rhythm
66
what type of rhythm does ghrelin have?
diurnal- this plays a role in meal regulation
67
How has ghrelin been proven to increase food intake?
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
what does PYY stand for?
peptide tyrosine tyrosine
69
where and when is PYY released?
from the terminal ileum and colon in response to feeding
70
what types of food induce best PYY response
wholegrain food, fish proteins + fibre
71
what does PYY do to appetite?
reduces it | -> can be digested or injected IV
72
whatt does PYY release inhibit release of?
NPY
73
which neurons are stimulated by PYY?
POMC
74
what can PYY cause at higher dose?
nausea and fullness | -> food intake reduction is dose dependent
75
examples of comorbidities obesity is associated with?
``` 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
How does environment and genetic susceptibility to obesity affect BMI?
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
what is the difference in how you observe leptin vs PYY satiety?
``` leptin = longer term PYY = immediate ```
78
Describe weight homeostasis
``` 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
How does leptin levels change with body fat? | How has this been scientifically proven?
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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