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Gastrointestinal biology > GIT hormones > Flashcards

GIT hormones Flashcards

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1
Q

What is the relation of the GI tract and the endocrine system?

A
  • Largest endocrine organ in the body.
  • Produces more than 20 substances that act as hormones or neurotransmitters.
  • Hormones are stored in specific peptide storage granules within cells, which are subsequently released by exocytosis.
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2
Q

What are the features of the endocrine cell?

A
  • Well-developed microvilli at the luminal border.
  • Secretory granules grouped towards the basal membrane.
  • They secrete only one hormone and are identified by letters (G cells, S cells, etc).
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3
Q

How are hormones related to communication?

A
  1. Endocrine – communicate with distant cells.
    - Transmitters are secreted into the bloodstream.
  2. Autocrine – communicate within the same cell
    - Some cells possess cell surface receptors for their own messengers.
  3. Paracrine – communicate with nearby cells
    - Act on neighbouring cells
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4
Q

List the major GI hormones.

A
  • Gastrin
  • Cholecystokinin (CCK)
  • Secretin
  • Others: Somatostatin, Motilin, serotonin.
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5
Q

What do Gastrin and Cholecystokinin (CCK) have in common?

A
  • Gastrin and CCK share a four aa C-terminal consensus sequence (Trp-Met-Asp-Phe-NH2), which is required for receptor activation.
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6
Q

What are the receptors of the gastrin family peptides?

A
  • 2 GPCRs found in vertabrae:
    1. CCK1 receptor (CCK1R)
    2. CCK2 receptor (CCK2R)
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7
Q

Discuss the binding of Gastrin and CCK to their corresponding receptor.

A
  • CCK1R is a CCK-specific receptor that binds sulphated CCK.
  • CCK and gastrin are CCK2R ligands with similar affinity and potency.
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8
Q

Where can we find CCK2 receptors?

A
  • On enterochromaffin-like cells and parietal cells
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9
Q

Where is gastrin produced and where does it act?

A
  • By cells called G cells in the antral portion of the gastric mucosa.
  • Receptors mediating gastrin responses to changes in gastric contents are present on the microvilli.
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10
Q

What stimulus increase gastrin secretion?

A
  • Peptides and amino acids
  • Gastric distension
  • Vagal stimulation
  • Presence of gastrin releasing peptide
  • Calcium
  • Epinephrine
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11
Q

What stimuli inhibit gastrin secretion?

A
  • Acid
  • Somatostatin
  • Secretin, GIP, VIP, glucagon, alcitonin.
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12
Q

What stimuli inhibit gastrin secretion?

A
  • Acid
  • Somatostatin
  • Secretin, GIP, VIP, glucagon, alcitonin.
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13
Q

What is the function of gastrin?

A
  • Stimulation of gastric acid and pepsin secretion.
  • Stimulation of the growth of the mucosa of the stomach and small and large intestines.
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14
Q

What are the proliferative effects of gastrin on gastric mucosa?

A
  • Causes gastric remodelling:
    1. Helps maintain well developed, functionally
    viable digestive tract lining.
    2. But may be involved in the development of
    gastric cancers
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15
Q

How does gastrin stimulate gastric acid secretion?

A
  • By direct binding on parietal cells
  • Or by a paracrine effect on the enterochromaffin-like cells, which then release histamine that activates the parietal cells.
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16
Q

How does Somatostatin inhibit gastrin?

A
  • The increased H+ feeds back to the D cells of the antrum to release somatostatin to turn off the gastrin release.
17
Q

Where is Cholecystokinin (CCK) released?

A
  • Secreted by I cells located in the mucosa of the upper small intestine (duodenum, jejunum)
  • Also made in the brain and the enteric nervous system.
  • Ingested fat and protein stimulate CCK release (sensed by GPR40 and the calcium-sensing
    receptor).
17
Q

What is the function of CCK?

A
  • Gallbladder:
    1. Stimulates contraction of the gallbladder (bile to flow with pancreatic juice)
  • Pancreas:
    1. Relaxes sphincter of Oddi (allows bile and pancreatic juice to flow between the pancreas
    and the small intestine).
    2. Stimulates secretion of pancreatic enzymes (lipases, amylase, and proteases).
    3. Secretion of bicarbonate from the pancreas.
  • Parietal cells:
    1. Indirectly decreasing secretion of acid binding to CCK1 receptors on D cells, stimulating release of somatostatin.
  • Inhibits gastric emptying.
  • CNS:
    1. CCK is implicated in anxiogenesis, satiety, appetite, memory, and learning.
18
Q

Where is the hormone Secretin released?

A
  • Secreted from S cells located in the duodenum.
  • Secretin release is stimulated by gastric acid delivered into the duodenal lumen.
  • Secretin is also released by digested products of fat and protein.
19
Q

What are the functions of secretin?

A
  • Neutralise acid in the intestine by effects on
    secretions from the pancreas and gallbladder:
    1. Pancreas: to secrete aqueous bicarbonate.
    2. Liver: to secrete bicarbonate rich bile.
  • Inhibits gastrin, gastric motility & acid secretion (via somatostatin):
    1. Prevent further acid from entering duodenum until acid already present is neutralised.
    2. Inhibits gastrin secretion to reduce amount of acid being produced.
20
Q

Where is Somatostatin released?

A
  • In the gut: by D cells in the gastric and intestinal mucosa.
  • Islets of the pancreas.
  • Enteric neurons.
21
Q

What stimulate release of Somatostatin?

A
  • CCK (CCK1 receptor) and ACh (muscarinic receptor) stimulate release in response to presence of acid in duodenum or increased
    blood glucose/amino acids.
22
Q

What is the function Somatostatin?

A
  • Suppresses all the activities GI tract:
    1. Low gastric pH stimulates D cells in antrum to produce somatostatin and inhibit gastrin release by a paracrine effect.
  • Reduces secretions from salivary glands, biliary tree, stomach, and pancreas.
  • Suppresses release: gastrin, secretin, motilin, enteroglucagon, CCK, VIP, GIP, intrinsic factor, pepsin, neurotensin, insulin, PP, and glucagon.
  • Inhibits GI motility, reduces visceral blood flow, & limits cell growth and renewal within GI tract.
23
Q

Where is Motilin released?

A
  • From “M” cells of the mucosa (duodenum, jejunum) during fasting to stimulate GI motility.
  • How: Fasting = fluctuating motilin levels. release in 90 min cycles and ^ GI motility (rumbling).
  • This helps clear intestine of foreign bodies & residual undigested material.
24
Q

How is the action of Motilin inhibited?

A
  • The cyclical release and action get inhibited by the ingestion of food.
25
Q

Where is serotonin (5HT) released?

A
  • Enterochromaffin cells in response to mechanical or chemical irritation of GI tract e.g. presence of drugs and toxins.
    -Results in ^ contractile activity e.g. emptying of a noxious substance form the GIT.
26
Q

What is the effect of excessive activation of vagal sensory afferent 5-HT3 receptors in chemoreceptor trigger zone?

A
  • Induces nausea and vomiting.
  • Blocking of 5 HT 3 receptors is very effective as an anti emetic.
27
Q

Where is gastric inhibitory polypeptide (GIP) released?

A
  • From K cells (duodenal mucosa) ) in response to the presence of food in the upper small intestine.
  • Also known as glucose dependent insulinotropic polypeptide.
28
Q

What is the function of GIP?

A
  • Mainly: Stimulation of insulin secretion (insulinotropic peptide).
  • Inhibits gastric acid secretion and motility - slows gastric emptying when the upper small intestine is full of food products (requires higher than normal physiological levels).
  • Only hormone that is released in response to all three types of food (fatty acids, carbs, amino acids).
29
Q

Where is vasoactive intestinal peptide (VIP) released?

A
  • Vasoactive peptide hormone and neuroendocrine peptide*.
  • Found in CNS and GIT.
30
Q

What is the function of VIP?

A
  • Induces smooth muscle relaxation (lower esophageal sphincter, stomach, sphincter of Oddi) - mediates distention induced reflexes.
  • Inhibition of gastric acid secretion.
  • Stimulates pancreatic bicarbonate secretion.

Gastrointestinal biology (24 decks)

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