Nutrient Sensing Flashcards
what is required for gastric acid secretion
gastrin
histamine
ACh
steps in gastric acid secretion
gastrin activates endocrine cells
endocrine cells release histamine
histamine directed to parietal cells with contain a proton pump (Ca2+/cAMP dependent)
proton pump exchanges H+ out, K+ in causing gastric acid secretion
vagus nerve releases ACh
ACh activates Gq GPCR which activates the proton pump
what forms the mucus layer
biocarbonate ions and mucus
pH of 7
what is the role of the prostoglandin receptor
prevents proton pump activation
what do G cells contain
located in the stomach
contain gastrin
what do L cells contain
neurotensin/GIP/GLP-1/2/OXM/PYY (bowel)
what do EC cells contain
5-HT/SP/Histamine
(GI area)
PYY
pro absorptive
anti secretory (retains electrolytes and inhibits electrolyte secretion)
defends against diarrhoea
mediates ileum and colonic brakes (slows motiliy)
GLP
pro absorptive
slows gastric emptying
proliferative/anti-apoptotic in GI tract
controls blood glucose and insulin secretion (incretins)
GLP-1 vs GLP-2
GLP-1 reduces bodyweight
GLP-2 glucose sensing
how does GLP-2 sense glucose in the enteric secretomotor neurons
glucose stimulates tastant receptors TIR2
GLP-2 released
GLP-2 stimulates VIP to cause electrolyte secretion
VIP released from varicosities
cAMP-CFTR-Cl- release
counter ion/electrolyte movement
where is GPR119 expressed
highly in the pancreas and GI tract
insulin secretion
‘fat sensor’, sensing endogenous and luminal N-acylethanolamines
in mouse ileum»colon>SI
L cell activity
glucose dependent/inhibited by phloridzin = SGLT1 inhibitor
role of GPR119
reduces hyperglycemia
improves glucose tolerance
increases PYY/GLP-1/GIP release
fat sensor senses endogeneous lipids
FFA2 (GPR43)
ligands: SCFA (C2/3)
Gi/Gq coupled
PYY and GLP-1 release, satiety, anti-inflammatory,adipogenesis, inhibits lipolysis
in L cells
