119 - Neuronal and Hormonal Control of the GIT 2 Flashcards
Effects of acid in the duodenum 1 2 3 4
1) D cells release somatostatin
2) Excites terminals of vagal afferent neurons to trigger vago-vagal reflex –> Brunner’s glands release mucus and bicarbonate.
3) Vago-vagal reflex inhibits gastric emptying
4) Duodenal-pyloro-antral reflex closes pylorus, also inhibits gastric emptying
Effect of somatostatin in the stomach
Acts on parietal cells via GPCR, reduces acid secretion
Example of a disease state where duodenal-pyloro-antral reflex is subverted
Gastroparesis
What release CCK in the duodenum?
I cells (subset of enteroendocrine cells)
Effect of CCK on neurons in the duodenum
1
2
1) CCK excites terminals of vagal afferent pathways to brain (EG: one goes to part of brain responsible for appetite, suppresses hunger)
2) CCK excites terminals of enteric sensory neurons (EG: initiation of segmentation process, part of fed-state motor pattern)
Secretin
Triggers secretion of bicarbonate-rich solution from pancreas
Effect of bicarbonate-rich solution from pancreas
1
2
3
1) Neutralise stomach acid in duodenum
2) Neutralising acid inactivates pepsin, stops somatostatin secretion from duodenal D cells.
3) Terminates acid-stimulated duodenal-antral reflexes and vago-vago reflexes (stops inhibition of gastric emptying)
Hormonal effects of CCK
1
2
3
1) Causes gall bladder to contract, forcing bile into duodenum
2) Releases enzymes from pancreas
3) Satiety factor that acts on hypothalamus to partly suppress appetite
Hormones that ensure proper environment for digestion in duodenum and jejunum
Secretin and CCK
How does CCK suppress appetite?
Excites vagal afferents via a paracrine effect.
May also act directly in hypothalamic regions without blood-brain barrier
Name for peristaltic wave from distal duodenum towards stomach
Retropulsion
Role of retropulsion at the same time as peristalsis
Mix chyme with bicarbonate-rich solution, pancreatic enzymes. Important in digestion.
Effect of failure of retropulsion
Can lead to peptic ulcers, as acid from stomach isn’t completely neutralised by bicarbonate
How is the status of the gut normally detected?
Mechanically, as the mucosa is a barrier to the diffusion of chemicals from lumen into the body
Example of a chemical signal that can diffuse directly across mucosa
Acid
Examples of cells in the gut that can detect chemical signals
Enterochromaffin cells, enteroendocrine cells
How do mucosal cells ‘taste’ the lumen?
Have the same pathways for bitter and umami
Result of stimulation of mucosal taste pathways
Tastants cause release of serotonin from enterochromaffin cells
Cells in mucosa that detect sweet tastes
L cells
Effect of L cells detecting ‘sweet’ tastes
1
2
3
1) Contain, release glucacon-like peptides 1 and 2, and pancreatic polypeptide Y
2) These hormones regulate insulin secretion (PYY) and insulin secretion
3) PYY also acts on enteric neurons
Emphasis of neural control between stomach and duodenum
In stomach, more emphasis is on vagus nerve.
In duodenum, more emphasis on enteric neural circuits
Distinct motor patterns when food is in the duodenum
1
2
3
1) Retropulsion – constrictions running towards pylorus – mixes pancreatic juices and bile with food activating and facilitating digestion
2) Segmentation – local constrictions alternating with relaxation – mix food with digestive enzymes and bile, also bring nutrients to absorptive epithelium
3) Peristalsis propels content into new regions of intestine
Transfer of food from duodenum to jejunum
1
2
3
1) Digestion releases nutrient molecules that activate EE and EC cells to modulate ratio of segmenting to peristaltic contractions
2) Rate of transit determines efficacy of digestion and absorption
3) Gastric emptying continues retriggering the basic processes (fat empties last, giving surge of CCK release, slowing transit, increasing food absorption)
Speed of bolus through duodenum to jejunum
Slow movement through segmentation.
Can move more quickly by peristalsis
Movement of food from jejunum to colon
1
2
3 a, b
• Basic mechanism the same, but stimuli change as digestion is completed
• Absorption of water makes content more viscous, altering feedback from muscle and increasing resistance to flow
• In proximal colon fermentation by the microbiome produces short chain fatty acids
– Acetate, butyrate, propionate
– All stimulate enteric reflexes
What stimulates urge to defecate?
Distension of of rectum triggers urge to defecate via sacral primary afferent neurons
What does defecation require to take place?
Conscious (cortical) neural activity to relax anal sphincter and contract abdominal muscles for normal defecation
Effect of irritable bowel syndrome on defecation
Threshold for stimulation of sacral afferents is decreased, leading to ability to sense content in rectum that isn’t normally detectable
Fasted state
1 a, b, c, d
2 a
3
• Neurally regulated interdigestive motor complex
– Also known as migrating motor complex (MMC)
– Wave of constriction initiated in antrum or upper duodenum propagates slowly to ileo-colonic junction
– Only one MMC constriction in small intestine at a time
– Possibly triggered by release of motilin, but many other hormones also released
• Clears bacteria and cellular debris from otherwise empty lumen
– Failure causes bacterial overgrowth
• Common issue post surgery, ileus
Other hormones in GIT
1
2
• Ghrelin – growth hormone release inhibitor
– Released from stomach in fasted state and stimulates appetite
–May initiate MMC
• Gastrin releasing peptide
– Found in nerve terminals near G cells
– Acts in parallel to vagally released acetylcholine
