Integrated response to a meal

Question 1

GPCRs for various GI affectors

Answer 1

• M3 ACh, gastrin, and CCK (cholecystokinin) receptors all stimulate phospholipase C-B (converts PIP2 -> IP3 + DAG), which ultimately leads to an increase in Ca
• B-adrenergic, H2 (histamine), secretin receptors all use AC to increase cAMP
• A-adrenergic receptor uses ADP-ribosyl cyclase to make cADP-R, which ultimately leads to a rise in Ca

Question 2

Cephalic phase

Answer 2

• Salivary gland stimulation in response to thought, smell, taste, act of chewing/swallowing
• Salivary glands are activated by both SNS and PsNS
• SNS activity on salivary glands causes them to secrete nzs (amylase and mucins)
• PsNS activity causes salivary glands to release NaCl + H2O

Question 3

Gastric phase 1

Answer 3

• Part stomach response and part pancreas response
• Both controlled by vagal efferents
• Vagus on stomach: stimualtes peristalsis, acid secretion, pepsinogen secretion, gastric secretion
• Vagus on pancreas: NaCl/H2O and zymogen secretion
• Upper part of stomach (body/fundus) for receptive relaxation, lower part (antrum) for mixing/emptying

Question 4

Gastric phase 2

Answer 4

• Oxynto-oxyntic (body-body connections) cause HCl secretions
• Oxynto-pyloric (body-antrum connections) cause gastrin secretion
• Pyloro-pyloric (antrum-antrum connections) cause gastrin release
• Pyloro-oxyntic (antrum-body connections) cause HCl release

Question 5

Intestinal motility

Answer 5

-PsNS increases, SNS decreases and dissension can either increase or decrease (depends on intensity)

Question 6

Hormonal control of GI 1

Answer 6

• Gastrin: secreted by stomach in response to neural signals (ACh, gastrin-releasing peptide), distension, AAs in stomach
• Target cell/response: gastric parietal cells to increase HCl secretion and gastric SmM to increase motility
• Secretin: secreted by SI (mucosal cells) in response to acid in SI lumen
• Target cell/response: pancreatic and hepatic duct cells to increase bicarb secretion, potentiates pancreatic acini response to CCK (which causes increased pancreatic nz/NaCl secretion)
• Also causes stomach to decrease emptying and decrease acid secretion

Question 7

Hormonal control of GI 2

Answer 7

• CCK: secreted by SI (mucosal cells) in response to AAs and FFAs in SI lumen
• Target cell/response: pancreatic acini to increase nz/NaCl secretion, potentiates pancreatic and hepatic duct response to secretin (to increase bicarb secretion), stimulates gallbladder to contract, decreases gastric emptying
• Bicarb release depends on secretin, plus CCK for potentiation of secretin’s effect
• NaCl/nz release depends on CCK, plus secretin for potentiation of CCK’s effect

Question 8

Control of gastrin release and gastrin’s effects

Answer 8

• ACh and gastrin-releasing peptide stimulation (neural) causes gastrin release
• pH<3 inhibits gastrin release
• AAs/peptides stimulate gastrin release
• Distension in stomach stimulates gastrin release
• ECL cells (mast cell-like) will release histamine upon activation by gastrin and ACh
• The histamine will bind to H2 receptors on oxyntic (parietal) cells, leading to increased HCl secretion
• Gastrin can bind to its receptor (as can ACh binding to M3) on the oxyntic cell to cause HCl release as well

Question 9

Gastic inhibitor peptid (GIP)

Answer 9

• Produced in mocusa of SI, released in response to FFAs and monosaccharides (doesn’t need AAs present)
• GIP cause parietal cells to decrease acid secretion
• It also potentiates pancreatic islet cells’ response to glc, thus increasing insulin release