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Endocrinology > Lec 14 - Gut hormones > Flashcards

Lec 14 - Gut hormones Flashcards

1
Q

2 types of enteroendocrine cells (EEC)

A
  • open EEC = has microvilli to sample the lumen
  • closed EEC = no access to lumen, recieve input from eihter blood or neurotransmitters from motor neurons
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2
Q

what do EECs do

A

release hormones in response to nutrints in gut lumen

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3
Q

what type of hromone are most GI hromones

A

peptides that bind to GPCRs

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4
Q

3 types of gut peptide hromones

A
  • gastrins = regulate digestive process
  • secretins = induce hormone release
  • motilins = regulate gastric motility
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5
Q

the 3 phases of hromone release

A
  • cephalic phase
  • gastric phase
  • intestinal phase
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6
Q

Cholecystokinin (CCK): where released from

A

I cells in duodenum

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7
Q

Cholecystokinin (CCK): when released

A

stimulated by fat and protein in intestinal lumen

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8
Q

Cholecystokinin (CCK): what receptor

A

CCK 1 receptor

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9
Q

Cholecystokinin (CCK): effects

A

decreased gastric motility
delayed gastric emptying
increased satiety (smaller meals BUT eat more frq, so food intake is acc the same = not used to treat obesity)

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10
Q

Glucose dependent insulinotropic polypeptide (GIP): wehre released from

A

K-cells in duodenum

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11
Q

Glucose dependent insulinotropic polypeptide (GIP): released why

A

stimulated by sugar and fat

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12
Q

Glucose dependent insulinotropic polypeptide (GIP): effects

A

Incretin horome release to increase insulin secretion from pancreatic beta cells

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13
Q

Glucose dependent insulinotropic polypeptide (GIP): what type of hormone

A

endocrine

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14
Q

Glucose dependent insulinotropic polypeptide (GIP): where does it act

A

on GIPR on beta cells in pancreas
- GIPR also throughout the body

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15
Q

Glucose dependent insulinotropic polypeptide (GIP): why doesnt it reduce food intake on its own effectively

A

doesnt reach the CNS cuz degraded so fast

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16
Q

Glucose dependent insulinotropic polypeptide (GIP): what do long acting GIPRA allow

A

long acting GIP agonists
allow bidning to GIPR in brainstem = reduce food intake and body weight

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17
Q

Glucagon like peptide-1 (GLP-1): where released

A

L - cells in ileum and jejunum

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18
Q

Glucagon like peptide-1 (GLP-1): when released

A
  • in cephalic phase = stimulated by neural input from brain
  • post-prandially is stimulated by sugar
19
Q

Glucagon like peptide-1 (GLP-1): effects

A
  • an incretin hromone: inc insulin release
  • decreases glucagon release
  • ileal brake = inhibit gastric emptying,
20
Q

Glucagon like peptide-1 (GLP-1): what type of hromone

A

endrocrine and neural

21
Q

Glucagon like peptide-1 (GLP-1): what does it do in the CNS

A

acts on ARC and AP to increase satiety

22
Q

Glucagon like peptide-1 (GLP-1): what receptor

A

GLP-1R

23
Q

Glucagon like peptide-1 (GLP-1): effects on vagal afferent neurons

A

triggers vago-vagal reflex
decreases gastric emptying
increases satiation

24
Q

enzyme that cleaves GLP-1, giving it a short half life

A

DPP4

25
Q

what are gliptins

A

DPP-4 inhibitors = inc circulating GLP-1

26
Q

what are exendins

A

analogues of GLP-1 that are resistant to DPP4

27
Q

primary fucntion of leptin

A

signals sufficiency of adipose stores to permit various biological functions

28
Q

leptin deficiency symptoms

A

obese
hyperphagic

29
Q

leptin receptor>

A

LepR
5 types, located peripherallly and centrally
receptor tyrosine kinases

30
Q

what does receptor tyrosine kinases trigger

A

JAK/STAT signalling pathways

31
Q

Leptin: what type of signalling

A

neural and endocrine

32
Q

how does leptin affect orexigenic and anorexignic signals

A
  • attenuates orex
  • potentiates anorex
    = induces satiety
33
Q

effect of circulating leptin binding to LepR in arcuate nucleus

A
  • inhibits AgRP/NPY
  • stimulates POMC neurons = release of aMSH
    = reduced food intake
    = increased energy expendature
34
Q

what might hyperleptinaemia lead to

A

leptin resistance

35
Q

leptin resistancce as a cause of obesity

A

rare
but can have congenital defect in leptin gene
OR
leptin receptor defects

36
Q

Ghrelin: released from where

A
  • Pd1 cells in stomach
  • X/A cells in enteroendocrine
  • episilon cells in islets of langerhans literally wtf is that
37
Q

Ghrelin: when stimulated

A

cephalic phase
empty stomach is major trigger for ghrelin

38
Q

Ghrelin: main function

A

the only HUNGER hormone
appetite stimulus
increases gastric motility
increases gastric acid secretion

39
Q

Ghrelin: effects of adminstering exogenous ghrelin

A

stim feelings of hunger
causes hunger pains, by contracting gi tract muscles

40
Q

Ghrelin: how does it signal

A

neural and endocrine pathways

41
Q

Ghrelin: what receptor

A

growth hormone secretagogue receptor (GHSR)

42
Q

Ghrelin: where are GHSR

A

either:
- vagal/sympathetic afferent neurons (neural)
- target tissues e.g. brain (endocrine)

43
Q

how does leptin control ghrelin

A

High adiposity = high leptin = inhibition of ghrelin = decreases hunger
And vice versa

44
Q

Ghrelin: in terms of endorcrine control, what does it act on

A

the GHSR in arcuate nucleus:
- stimulates AgRP/NPY neurones
- inhibits POMC neurons

Endocrinology (25 decks)

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