Gastrointestinal hormones are secreted in the GI tract to facilitate digestion. The major classifications include gastrin family hormones like gastrin and CCK, secretin family like secretin, and others like ghrelin. Gastrin increases stomach acid and motility. Histamine also increases stomach acid production when stimulated by gastrin. Secretin regulates bicarbonate and pancreas secretions. Hormone release is controlled through neural and endocrine pathways involving feedback loops between the stomach, pancreas, and duodenum.

1. Gastrointestinal
hormone

2. Gastrointestinal hormone
CLASSIFICATION
Is a group of hormones secreted in the
gastrointestinal tract in order to facilitate the
conversion of food but molecular forms can travel
into the bloodstream process

3. Gastrointestinal hormone
CLASSIFICATION
GASTRIN
FAMILY
•1. Gastrin
•2. Cholecystokinin
SECRTIN
FAMILY
•1. Secretin
•2. Glucagon
•3. Glicentin
•4. VIP
•5. GIP
OTHERS
•1. Peptide
•2. Ghrelin
•Motilin3.
•4. Somatostatin
•5. Neurotensin
•6. Substance P
•7. GRP
•8. Bombesin
•9. Glucagon
•10.Guanylin

4. Functions of the GI Tract
 Ingestion: Taking in food
 Digestion: Chemical and Mechanical
 Absorption: moving nutrients from the lumen of
the GI tract into the cells of the body
 Excretion: getting rid of undigested and
unabsorbed material
 Movement: movement of ingested food
throughout the GI tract

5. Organs of the Digestive System
 Accessory Digestive Organs:
Salivary glands
Liver, gall bladder
Pancreas
 Digestive Tract:
Oral Cavity
Pharynx
Esophagus
Stomach
Small Intestine
Large Intestine

6. The Oral Cavity
 Boundaries are:
- lips (anteriorly)
- cheeks (laterally)
- palate (superiorly)
 The oral cavity is important in:
- mastication (chewing): mechanical digestion
- secretion of saliva for digestion (amylase; digests starch),
coating food (mucus)
- no significant absorption of nutrients occurs in the oral
cavity

7. The Pharynx
 The pharynx is the passageway from the nose and mouth to
the esophagus and respiratory tract
 Boundaries: uvula to epiglottis
 During swallowing, food is directed from pharynx to
esophagus (away from respiratory tract

8. Esophagus
 The esophagus is a passageway from the
pharynx to stomach
 Contains two sphincters: upper and lower
esophageal sphincters (controls flow)
 Upper sphincter is skeletal (voluntary), lower
sphincter is smooth muscle (involuntary)
 Peristaltic waves move food from pharynx to
stomach.

9. The Stomach
The stomach stores food, and mixes and mechanically and
chemically digests it
The stomach also secretes digestive juices
pepsin: digests protein
hydrochloric acid (acidic pH, required for pepsin activity, and
to kill ingested bacteria)
Mucus: protects the stomach wall
Partially digested food: chyme
Little absorption occurs in the stomach (exceptions: alcohol,
aspirin…)

10. Histology of the Stomach
 Cell types:
Chief cells: produce pepsinogen (inactive precursor to pepsin)
Parietal cells: produce HCl and intrinsic factor (absorption of vitamin
B12; important in RBC maturation)
“Endocrine” cells:
G cells: gastrin
D cells: somatostatin (paracrine)
Enterochromaffin-like cells: histamine

11. Small Intestine
 Connects the stomach with the large intestine
 It is the major site of digestion
 It is also the major site of absorption
 Specialized structures (villi, microvilli) increase the surface area of
the small intestine, aiding absorption.
 The small intestine has three parts (duodenum, jejunum, and
ileum)
 The bile duct (from liver) and pancreatic duct (digestive juices)
empty into the duodenum.

12. Histology of the Small Intestine
 Absorptive cells
 Goblet cells (mucus)
 Enteroendocrine cells:
secretin
cholecystokinin

13. Digestion & Absorption: Carbohydrates
Carbohydrates: small amount of digestion begins in oral cavity
(amylase). Most digestion in small intestine:
Enzyme Digests
pancreatic amylase polysaccharides to
disaccharides
disaccharidases disaccharides into (small intestine)
monosaccharides
What’s absorbed: monosaccharides

14. Digestion & Absorption: Proteins
Proteins: Digestion begins in stomach (pepsin), continues in small
intestine:
Enzyme Digests
trypsin, chymotrypsin, polypeptides into
carboxypeptidase small peptides
(from pancreas)
aminopeptidase
dipeptidases small peptides
into smaller peptides
What’s absorbed: mono-, di-, and tri-peptides

15. Digestion & Absorption : Lipids
Lipids: Digestion begins in the small intestine (minor amount in oral
cavity)
Note: Lipids are not soluble in water. Thus, it is hard for enzymes
to act on them.
 The first step in lipid digestion is emulsification of lipids with bile
(secreted from the liver).
 Emulsification: transformation of large lipid droplets into small
lipid droplets.
 This increases the surface area of lipid that can be acted on by
the digestive enzyme, pancreatic lipase.

16. Emulsification of Lipids by Bile
 Bile acts on lipids in a way similar to detergent
acting on greasy water:
large lipid droplet
bile

17. Absorption of Lipids
 Bile also helps absorption of products of lipid
digestion, forming micelles (free fatty acids,
glycerol, cholesterol).
 Absorption of lipids is required for absorption
of fat-soluble vitamins (vitamins A, D, E, K)

18. Digestion and Absorption: Nucleic Acids
 Food also contains RNA and DNA (also from shed cells of the GI
tract).
 The pancreas releases nucleases into the small intestine.
 Nucleases digest RNA and DNA into components.
 Digestion and absorption of dietary nucleic acids probably not
important for DNA/RNA synthesis

19. Absorption in the Small Intestine: Water
 About 9 liters of water enters the digestive tract
each day.
 About 8 liters of this is absorbed by the small
intestine (by osmosis, following movement of
ions).

20. Large Intestine
 Last portion of the digestive tract.
 No digestion occurs in the large intestine.
 In the large intestine, there is absorption of water
(about 1 liter/day) and salts from feces
(undigested, unabsorbed food).
 Bacteria produce vitamin K, B vitamins.
 Secretion of mucus (lubrication of feces)
 Contractions move feces along large intestine and
rectum, to be expelled out of the anal canal.

21. Accessory Digestive Organs
 Pancreas: exocrine portion produces digestive
enzymes, bicarbonate
 Liver: Produces bile, stores glycogen,
interconverts nutrients (gluconeogenesis),
detoxifies toxic substances (alcohol, drugs,
ammonia…), makes blood proteins (albumin,
fibrinogen, clotting factors)
 Gallbladder: concentrates and stores bile

22. Regulation of Digestion
 Allow communication between different parts of
the digestive tract
 Ensure the presence of sufficient secretions when
food present
 Help avoid overabundance of secretions in
absence of food
 Two types of mechanisms: neural and endocrine

23. Neural Control of Digestion
 Neural control of digestion is controlled largely
by the parasympathetic nervous system, and
local (enteric) reflexes.
 Activation of the parasympathetic system results
in secretion of digestive juices, increased motility
of the stomach, and slowing down movement of
food from the stomach to small intestine.

24. Neural Control of Digestion
 Stimuli: Thought, sight, taste of smell of food;
distension of GI tract; chemoreceptors detecting
nutrients, pH.
 Example: Thought, chewing, or taste of food
activates parasympathetic system, resulting in
increased release of mucus, HCl, and pepsin in the
stomach.
The goal of this is to prepare the stomach for
oncoming food.

25. Intestinal Phase of Gastric Secretion
(~ 10% of total)
(due to some G cells extending from antrum into the
duodenum)
Important aspect of intestinal phase is feedback regulation
and inhibition
Involves interactions between duodenal contents and
duodenal hormones, including their actions on pancreas, liver,
gall bladder, and stomach

26. G
gastrin
circulation
HCl
vagus
nerve
FOOD
Distension
Peptides
2. Gastric Phase of
Gastric Secretion
(approx 60% of total)
(initiated by gastric events)
G
gastrin
circulation
HCl
vagus
nerve
1. Cephalic Phase of
Gastric Secretion (approx.
30% of total)
(initiated by brain)
B. Functional Phases of Gastric Secretion

27. C. G.I. HORMONES
Structure of Secretin (27 AA)
(comparison with other GI hormones)
Gastrin (17 AA)
Cholecystokinin (CCK (33 AA))
+H+
+psnogn
+motil.
+LES
+growth
+panc enz
+G.B.
+growth
-Oddi
-gastr emptying
-synrg w/ Secretin
+HCO3 output
+psnogn
+synrg w/ CCK
-gastr emptying
-H+

28. Endocrine Control of Digestion
 Gastrin:
- produced from the stomach (G cells)
- release increased by stomach distension, peptides, amino
acids, alcohol, caffeine, parasympathetic innervation
- release inhibited by highly acidic pH (< 2.0)
- functions: increases gastric (stomach) secretions (primarily
HCl); increases histamine release; increases gastric motility; opens
pyloric sphincter (between stomach and small intestine), relaxes
ileocecal sphincter, stimulates growth of gastric mucosa.

29. Endocrine Control of Digestion
 Histamine:
Produced by enterochromaffin-like cells (ECL cells)
of the stomach.
Release is stimulated by gastrin.
Action: increase HCl secretion from parietal cells
(major factor in HCl secretion).

30. H/K
P
H/K
P
histamine-
secreting cell
Acetylcholine
neural input
neurocrine
Gastrin
hormonal input
endocrine
PARIETAL cell
paracrine
release of
histamine
histamine
receptor
ACh
receptor
gastrin
receptor
transduction-
activation events
HCl
secretion
Combined neurocrine, endocrine and paracrine
events in the activation of gastric HCl secretion
ECL cell
G cell
ECL cell =
enterochromaffin-like cell
G cell =
gastrin-secreting cell
HOW IT WORKS AT THE RECEPTOR LEVEL

31. H/K
P
H/K
P
histamine-
secreting cell
Acetylcholine
neural input
neurocrine
Gastrin
hormonal input
endocrine
PARIETAL cell
paracrine
release of
histamine
histamine
receptor
ACh
receptor
gastrin
receptor
transduction-
activation events
HCl
secretion
Combined neurocrine, endocrine and paracrine
events in the activation of gastric HCl secretion
ECL cell
G cell
ECL cell =
enterochromaffin-like cell
G cell =
gastrin-secreting cell
HOW IT WORKS AT THE RECEPTOR LEVEL
H-2 receptor blockers
H/K ATPase pump inhibitors
Tagamet
Zantac
Pepcid
Prilosec
Nexium
Aciphex

32. Turning the G-cell On
and Off
ACh ACh
ACh GRP
(Somatostatin)
cell
(Gastrin)
cellSS
GRP
neuron
digested
protein
H+
vagus
nerve
Circulating
Gastrin
GD
+-
++
cholinergic
neuron
gastric
mucosa
Gastric LumenGastric Lumen

33. Turning the G-cell On
and Off
ACh ACh
ACh GRP
(Somatostatin)
cell
(Gastrin)
cellSS
GRP
neuron
digested
proteinH+
vagus
nerve
Circulating
Gastrin
GD
+
++
cholinergic
neuron
gastric
mucosa
Gastric Lumen
SS = somatostatin
-

34. Endocrine Control of Digestion
 Somatostatin
Produced by D cells of the stomach
Secretion is stimulated by activation of the sympathetic nervous
system and by acidic pH, and is inhibited by activation of the
parasympathetic nervous system, continuously released,
overridden by gastrin and nerves.
Actions: inhibit gastrin and histamine secretion (decreased acid
release and gastric motility); also directly inhibits acid release
from parietal cells.

35. Endocrine Control of Digestion
 Secretin:
- Produced by duodenum (enteroendocrine cells of the small intestine);
crypts of Lieberkühn
- stimulated by arrival of acidic chyme in duodenum.
- functions: stimulates bicarbonate secretion from pancreas; inhibits
gastric secretion (decreases HCl production by inhibiting gastrin
release); decreases gastric motility (slowing rate of gastric digestion
and delivery to the small intestine), increases hepatic bile production,
increases CCK, promotes growth and maintenance of the pancreas.

36. Endocrine Control of Digestion
 Cholecystokinin (CCK):
- produced by enteroendocrine cells of the duodenum
- release stimulated by fatty acids in duodenum (also amino
acids, acidic chyme)
- functions: causes gallbladder contraction (bile to small
intestine); stimulates release of pancreatic enzymes; decreases
gastric motility and secretion (increases somatostatin release).

37. Endocrine Control of Digestion
Gastric Inhibitory Peptide (GIP):
Secretion: Enteroendocrine cells in the small intestine mucosa Crypts of
Lieberkuhn
Stimulus: Chyme rich in triglycerides, fatty acids, and glucose enter the
small intestine.
Actions:
 Stimulates release of insulin by beta cells
 Inhibits gastric secretion and motility
 Stimulates lipogenesis by adipose tissue
 Stimulates glucose use by skeletal muscle cells

38. Endocrine Control of Digestion
Vasoactive Intestinal Peptide (VIP):
Secretion: Enteroendocrine cells in the small intestine mucosa
Crypts of Lieberkuhn
Stimulus: Chyme entering the small intestine.
Actions:
 Stimulates buffer secretion
 Inhibits gastric secretion
 Dilates intestinal capillaries

39. Control of Gastric Acid Secretion
 How does a parietal cell secrete hydrochloric acid?
CO2 + H20 H2CO3 H+ + HCO3
-
Cl-
Cl-H+
HCO3-

40. Control of Gastric Acid Secretion
ECL
parietal
cellG Cell
HCl
Gastrin
histamine
D Cell
somatostatin (-)SECRETIN
CCK

41. Integration of Neural and Endocrine
Functions: Central Effects
 CNS: Thoughts, taste, smell of food; chewing – activates
parasympathetic nervous system (neurotransmitter: acetylcholine).
 ACh acts directly on parietal cells to increase acid secretion.
 Ach increases gastrin release, inhibits somatostatin release
(increased gastric secretion and motility).
 Sympathetic input (activity, stress): increased somatostatin release
(inhibiting gastrin secretion – decreased gastric secretion and
motility)

42. Integration of Neural and Endocrine
Functions: Local Reflexes
 Mechanoreceptors in the walls of the GI tract detect movement of food
into an organ
Example: In the stomach distension causes activation of the
parasympathetic system, increasing gastrin secretion and acid release,
and decreasing somatostatin secretion.
 Chemoreceptors detect nutrients and pH.
Example: Presence of amino acids, alcohol, or caffeine in the stomach
increases gastrin release.
Presence of fatty acids in the duodenum causes release of CCK.

43. Signaling Mechanisms
 Histamine: Receptor coupled to Gs – increases cyclic AMP production
and acts via PKA. Results in phosphorylation and increased
transport of proton pumps to cell membrane.
 Gastrin: Receptor coupled to Go/IP3/DAG; increased intracellular
calcium, and activation of PKC (PKC also phosphorylates proton
pumps).
 Somatostatin: Receptor coupled to Gi – inhibits cyclic AMP
production, decreasing PKA signaling.

44. Signaling Mechanisms
 CCK: Receptor coupled to Go (increased calcium causes
somatostatin release)
 Secretin: Receptor couple to Gs (increased cyclic AMP,
causes increased secretion of bicarbonate from the
pancreas)

45. Integration of
Gastric Secretion
+
+
+
+
+
+

46. Integration of Gastric
Secretion
+
-
- -
+
++
+
+

47. D. Duodenal Integration & Control: 1. Response to Acidity
Regulation by Secretin
HCl + NaHCO3 NaCl + CO2 + H2O
+
+
-
+
gall
bladder
liver
HCl
HCl
motility
NaCl
+ H2O
HCO3
HCl

48. Regulation by CCK (Cholecystokinin)
gall
bladder
Bile
FOOD
+
-
liver
+
fats &
peptides
bile &
enzymes
fat &
protein
digestion
- HCl
2. Duodenal Response to Food