Intro to GI physio Flashcards
somatostatin
in GI tract: released by D cells in response to low pH, inhibits H secretion and other GI hormones
outside GI tract: released by delta cells of pancreas and hypothalamus
Histamine
in the stomach: stored and secreted by enterochromaffin cells (in glands). acts on Parietal cells to increase H production
stimulates acid production
Gastrin
hormone family
site of secretion
stimuli of secretion
gastrin-cck
G cells of stomach
small peptides and a.a.
distention of stomach
vagal stimulation
Cholecystokinin (CCK)
hormone family
site of secretion
stimuli of secretion
gastrin-CCK
I cells of the duodenum and jejunum
small peptides and AA
FAs
pancreatic enzyme secretion
pancreative HCO3 secretion through potentiation of CCK (not a direct effect, it potentiates effects of secretion)
stimulation/contraction of gallbladder and relaxation of the spnicter of Oddi
stimulates growth of the exocrine pancreas and gallbladder (trophic effects)
inhibits gastric emptying
can also act as a paracrine signal
Secretin
hormone family
site of secretion
stimuli of secretion
secretin-glucagon
S cells of the duodenum
H in the duodenum, FAs in the duodenum
Glucose-dependent insulintropic peptide
secretin-glucagon family
duodenum and jejunum
FAs, a.a’s, oral glucose
Gastrin’s actions
stimulates acid secretion and mucosal growth
Zollinger-Ellison syndrome
gastrin secreting tumors
hypertrophy of gastric mucosa
duodenal ulcers
steatorrhea (fatty stools), pancreatic release is reduced
CCK actions
pancreatic enzyme secretion
pancreative HCO3 secretion through potentiation of CCK (not a direct effect, it potentiates effects of secretion)
stimulation/contraction of gallbladder and relaxation of the spnicter of Oddi
stimulates growth of the exocrine pancreas and gallbladder (trophic effects)
inhibits gastric emptying
can also act as a paracrine signal
secretin actions
increases pancreatic HCO3 secretion increases biliary HCO3 secretion decreases H secretion inhibits trophic effect of gastrin on gastric mucosa can also act as a paracrine signal
GIP actions
increases insulin secretion from pancreatic beta cells and decreases H secretion
oral glucose consumption is much more efficient way of releasing insulin than intravenous injection
ACh in the GI tract
source, action
cholinergic neurons
actions include salivary secretions, pancreatic secretions, gastric secretions
norepinephrine (NE)
source, action
adrenergic neurons
relaxation of smooth muscle
contraction of sphincters
increases salivary secretion
vasoactive intestinal peptide (VIP)
source, action
neurons of the mucosa and smooth muscle
actions include relaxation of smooth muscle
increase in intestinal secretion
increased in pancreatic secretion
GRP
source, acrion
gastrin releasing peptide
neurons from gastric mucosa
increases gastrin secretion
Enkephalins
neurons of the mucosa and smooth muscle
causes contraction of smooth muscle and decreases intestinal secretion
Neuropeptides Y
Neurons of the mucosa and smooth muscle.
relaxation of smooth muscle. decrease intestinal secretion.
substance P
Co-release with ACh
contraction of smooth muscle, salivary secretion
neuronal centers that control feeding and satiety are located in the
hypothalamus
Lateral nuclei (LH)
feeding center in the hypothalamus
ventromedial nuclei (VM)
satiety center
PDA
paraventricular nuclei
dorsomedial nuclei
arcuate nuclei
all hypothalamic centers involved in food intake
what stimuli are needed for hormone release?
physiological (food, acid, paracrine stimulation, glucose etc)
what stimuli are needed for NT release?
action potentials
alpha-MSH pw
neurons in arcuate nucleus secrete alpha-melanocortin (a-MSH) by pro-opiomelanocortin neurons (POMC)
alpha-MSH binds to MCR-4 present in second order neurons to INHIBIT food intake and increases metabolism
“big picture” a-MSH
inhibits food intake and increases metabolism
Neuropeptide Y pw
neurons in arcuate nucleus are stimulated by hunger signals to release NPY
NPY binds to Y1R
neurons that release NPY also release agouti-related peptide
AGRP is an antagonist of MCR-4
increases feeding behavior and storage of calories
alpha-MSH and NYP/AGRP are
antagonists: peptides from one inhibit the other system.
AGRP is an MCR-4 antagonist.
obesity
some cases have been related to mutation in the POMC and MCR4 genes
POMC
neuron in the arcuate hypothalamus: releases alpha-MSH to MCR-4 and inhibits food intake
the “vagal” circuit (basic components)
vagus–> NT—> hypothalamus
Ghrelin
secreted mainly by endocrine cells in the stomach
binds to growth hormone, secretagogue receptors
in the hypothalamus it stimulates neurons that release NPY
stimulates neurons that release NPY (big one)
other actions include increasing:
appetite gastric motility gastric acid secretion adipogenesis insulin secretion
appears to initiate the feeding response
insulin
transported across the blood brain barrier
binds to receptors in satiety and hunger centers within the hypothalamus (POMC and NPY systems)
actions:
decreasing appetite
increasing metabolism
in patients with type I diabetes mellitus, there is an increase in food intake associated with the decrease in insulin
CCK and Peptide YY
CCK released by I cells in the duodenum elicits satiety
CCK —> vagal —> NTS —> hypothalamic circuit –> decrease in ghrelin, decrease in gastric emptying
PYY released by EECs
released by EECs (L cells) of the ileum and colon
binds to Y2 receptors of the hypothalamus, which inhibits NPY neurons and released inhibition of POMC neurons
potential as appetite suppressor
Leptin
secreted by cells in adipose tissue and by endocrine cells in the stomach
binds to receptors in satiety and hunger centers within the hypothalamus (POMC and NPY systems)
appetite suppressing hormone:
decreases appetite
increases metabolism
decreases ghrelin
appears to be part of negative feedback system for the regulation of food intake
Paracrines
peptides secreted by endocrine cells of the GI tract
act locally
somatostatin
histamine
hormones
peptides released from endocrine cells of the GI tract through the portal circulation, through the liver, and enter systemic circulation
gastrin
CCK
secretin
GIP
Neurocrines
synthesized by neurons of the GI tract and released following an action potential
ACh NEP VIP GRP enkephalins NPY substance P
Criteria for a GI hormone
substance must be secreted in response to physiologic stimuli
function must be independent of neural activity
it must be isolated, purified, and chemically identified, and synthesized
only four qualify: CCK, secretin, gastrin, GIP
