3. Characteristics of GI peptides
• Water and electrolyte secretion
• Enzyme secretion
• Contraction and relaxation of the smooth muscle
• Regulate the release of other endocrines
• Have trophic effects
5. Fig: Classification of gastrointestinal peptides as hormones,
paracrines or neurocrines. GI, Gastrointestinal; R, Receptor.
6. Hormones
• Greek : ‘‘to set in motion’’
• Major GI hormones:
i) Secretin
ii) Gastrin
iii) Cholecystokinin- Pancreozymine (CCK-PZ)
iv) Gastric inhibitory peptide (GIP)
v) Motilin
7. • Some criteria must be satisfied to prove the
existence of a GI hormone:
(1) Substance must be secreted in response to a
physiologic stimulus and be carried in the
bloodstream to a distant site, where it produces
a physiologic action.
(2) Function must be independent of any neural
activity.
10. Figure: Principal sites of gastrointestinal hormone release.
• CCK: Cholecystokinin
• GIP: Glucose dependent insulinotropic peptide
11. Gastrin
• Source: G cells, mainly in antral region.
• Types: Two types of gastrin physiologically
important:
G34: big gastrin, found in the interdigestive state.
G17: little gastrin; accounts for about 90% of the gastrin
found in antral mucosa.
• Stimulus: Products of protein digestion, distention
of the stomach by food and vagal stimulation
• Metabolism: t1/2 of G34 = 38 minutes
t1/2 of G17 = 7 minutes
13. Gastrin contd..
• Functions:
1. Stimulation of gastric acid secretion from parietal cells
and pepsin secretion.
(Therefore, hypergastrinemia causes peptic ulcer.)
2. Trophic action of gastrin.
3. Stimulates gastric motility and exocrine pancreas
secretion.
4. Prevents reflux esophagitis.
14. Functions contd..
5. Stimulates insulin secretion.
6. Causes colonic contraction that initiates
gastrocolic reflex after a meal.
7. Stimulates histamine secretion from ECL
(enterochromaffin like cells) in GI mucosa.
16. Cholecystokinin
• Source: I cells in the mucosa of upper small
intestine.
• Stimulus: Fatty acids, monoglycerides, peptides
and amino acids.
• Metabolism: t1/2 = 5 minutes
17. • Functions of CCK:
1. Stimulates contraction of gallbladder.
2. Stimulates pancreatic secretion rich in enzymes.
Therefore, CCK is also called cholecystokinin-pancreozymin (CCK-
PZ).
3. Inhibits gastric acid secretion.
4. Inhibits gastric motility, thereby delays gastric
emptying.
5. Causes relaxation of sphincter of Oddi.
18. Functions of CCK
6. Stimulates growth of exocrine pancreas and gall
bladder.
7. Augments (increases) contraction of pyloric
sphincter.
8. Stimulates glucagon secretion.
9. In brain, acts as an anorexigenic neurotransmitter.
20. Secretin
• Source: S cells of Duodenum.
• Stimuli: Acid and fats.
• Functions:
1. Increases secretion of pancreatic juice rich in
bicarbonate and bile secretion.
2. Inhibits effects of gastrin on parietal cells.
3. Decreases gastric acid secretion and motility.
21. Glucose-dependent insulinotropic
polypeptide (GIP)
• Also known as Gastric Inhibitory Peptide
• Source: K cells present in the mucosa of duodenum
and jejunum.
• Stimuli: Carbs, fatty acids and peptides
• Functions:
1. It inhibits gastric secretion and motility.
2. It stimulates insulin secretion.
• Regulation of GIP secretion:
- Secretion is increased by glucose and fat in the
duodenum.
22. Motilin
• Source: Mo cells
• Released approximately every 90 min during
fasting.
• Functions:
1. Increases GI motility, especially in the
interdigestive phase.
2. Major regulator of migrating motor complex
(MMC).
24. Paracrines
• Synthesized in the endocrine cells of the GI tract.
• Do not enter the systemic circulation
• Act locally, reaching their target cells by diffusing
over short distances.
25. Neurocrines
• Synthesized in cell bodies of gastrointestinal
neurons.
• Action potential in the neuron
Causes release of the neurocrine that diffuses
across the synapse
Interacts with receptors on the postsynaptic cell
28. References
• Harvey, Richard A., Ph. D. (2011). Lippincott's
illustrated reviews: Biochemistry. Philadelphia :
Wolters Kluwer Health, Pg 379-381.
• Costanzo, L. S. (2011). Physiology. Philadelphia:
Wolters Kluwer Health/Lippincott Williams &
Wilkins, Pg 342-348
• Johnson Leonard R.(2003). Essential Medical
Physioogy. San Diego, California : Elsevier, Pg
468-476