Gut Signaling Flashcards
Nervous systems in the gut
Parasympathetic, Sympathetic, and Enteric
Neurotransmitters in the gut
Acetoylcholine, norephinephrine, vasoactive intestinal peptide (VIP), gastrin-releasing peptide (GRP), enkephalins (opiates), neuropeptide Y, Substance P
Acetylcholine source/action
cholinergic neurons; contract smooth mm, relax sphincters, increase salvitory/gastric/pancreatic secretions
Norepinephrine source/action
adrenergic neruons; relax smooth mm, contract sphincters, increase salivary sectretion
VIP source/action
mucosa neurons and smooth mm; relax smooth mm, increase intestinal and pancreatic secretion
GRP source/action
gastric mucosa neurons; increase gastrin secretion
Enkephalins source/action
neurons of mucosa and smooth mm; contract smooth mm, decrease intestinal secretion
Neuropeptide Y source/action
neurons of mucose and smooth mm; relax smooth mm, decrease intestinal secretion
Substance P source/action
consecrated with ACh; contract smooth mm, increase salivary secretion
Gastric hormones include:
gastrin, cholecystokinin (CCK), secretin, and glucose-dependant insulinotropic peptide (GIP)
Gastrin source
secreted by G cells in antrum of stomach in response to eating a meal (high phenylalane and tryptophan content) dissension of stomach, vegal stimulation (via GRP)
Gastrin form/action
secreted as either a 17 or 34 aa peptide, 17 while eating and 34 while fasting; promotes H+ secretion and growth of gastric epithelium
Zollinger-Ellison syndrome
Excess H+ secretion (duodenal ulcers and inactivates pancreatic lipase [poor fat digestion]) and hypertrophic gastric epithelium due to excess gastrin (think opposite effects in antrum resection). Usually caused by gastrinoma in non-Beta cell pancreas.
Tx Zollinger-Ellision syndrome
cimetidine (H2 receptor blocker) and omeprazole (H+ pump inhibitor). Gastric resection in extreme cases
CCK source
33aa peptide secreted by I cells in the duodenum and jejunum in response to monoglycerides and fatty acids (not TG though) as well as small peptides and amino acids [hey fat ass you just ate!!! signal]
CCK action
stimulates pancreas enzyme and bicarb secretion, gallbladder emptying, relax Oddi sphincter. Also stimulates exocrine pancreatic and gallbladder growth. Inhibits gastric emptying (hey fay ass you ate too much…. hold on a second!!!)
Pancreatic enzymes
lipases, proteases, and amylases
CCK-Gastrin relationship
both have same 5aa terminal sequence with some crossover effects
Secretin source
27 aa peptide resembling glucagon secreted by S cells of duodenum in response to H+ and fatty acids in lumen (pH
Secretin action
promote pancreatic bicarb secretion to neutralize acid (can’t digest fats in high acid environment [need pH 6-8]) also inhibits gastrin effects on parietal cells (H+ secretion) (the basic bitch gut hormone)
GIP source
42 aa peptide secreted from K cells in duodenum and jejunum in response to glucose, aa, and fatty acids.
GIP action
stimulates insulin secretion (reason oral glucose elicits greater insulin response) as well as inhibit H+ secretion from gastrin
GIP action
stimulates insulin secretion (reason oral glucose elicits greater insulin response) as well as inhibit H+ secretion from gastrin
Motilin
22aa peptide which increases gut motility (90minute intervals)
Pancreatic polypeptide
36aa peptide secreted in response to carb/protein/fat digestion and inhibits pancreatic bicarb secretion. (why? no one knows… the shadow knows!!!)
Enteroglucagon
released from intestinal cells in response to hypoglycemia. directs liver glyconeogensis
Somatostatin secretion
secreted by D cells of intestinal mucosa in response to decreased luminal pH
Somatostatin action
inhibits secretion of other gastrointestinal hormones as well as inhibiting gastric H+ secretion (paracrine)
Histamine secretion/action
secreted by H+ secreting region of the stomach; stimulates H+ secretion by gastric parietal cells (paracrine)
