GASTRIC ENDOCRINOLOGY

The gastrointestinal tract is the largest endocrine organ in the body, with its component cells dispersed along its
length rather than being clustered in glands.
Gut peptides integrate gastrointestinal function by regulating the actions of the epithelium, muscles, and nerves,
affect the growth and development of the gut and—as has emerged comparatively recently—they also have a major
role in appetite control.

Gastrin
 Source
 G cells in the stomach.
 Trigger
 Protein and amino acids stimulate gastrin secretion but somatostatin and acid suppresses gastrin
secretion.
 Action
 Increases gastric acid secretion.

Somastatin
 Source
 D cells which are located throughout the gastrointestinal tract (gut).
 Trigger
 Eating fatty foods.
 Actions
 Reduces gastrin and stomach acid secretion.
 Inhibits insulin and pancreatic enzyme secretion.
 Decreases nutrient absorption from the gut.

Grehlin
 Source
 Stomach
 Trigger
 Secretion stimulated by fasting or starvation and suppressed by eating food.
 Action
 Stimulates appetite.

Cholecystokinin (CCK)
 Source
 First two parts of the small intestine (duodenum, jejunum) – I cells.
 Nerve endings in the last part of the small intestine (ileum) and colon.
 Triggers
 Protein and amino acids.
 Fatty foods.
 Trypsin which is a pancreatic enzyme that assists with the digestion of proteins suppresses the
secretion of CCK.
 Actions
 Feeling of satiety which reduces appetite.
 Reduces gastric acid secretion and gastric emptying (passing of food from the stomach into the
duodenum)
 Stimulates pancreatic enzyme secretion.
  Stimulates gallbladder contraction and bile flow.
 Opens the sphincter of Oddi which allows the pancreatic enzymes and bile to enter the small
intestine.

Secretin
 Source
 First two parts of the small intestine (duodenum, jejunum) – S cells.
 Triggers
 Acid in the duodenum (small intestine) – increase in pH.
 Fatty acids.
 Actions
 Stimulates pancreatic fluid and bicarbonate secretion for the dilution and neutralization of stomach
acid in the small intestine.
 Decreases gastric acid secretion.
 Reduces gastric emptying (passing of food from the stomach into the duodenum).

Motilin
 Source
 Small intestine
 Colon
 Triggers
 Fasting, starvation.
 Fatty foods.
 Actions
 Controls peristalsis by stimulating smooth muscle contraction and relaxation to coordinate the
movement of food through the gut.
 Regulates movement of residual undigested material through the gut between meals.

Gastric Inihibitory Polypeptide (GIP)

 Source
 Duodenum and jejunum – K cells.
 Triggers
 Glucose.
 Fatty foods.
 Actions
 Reduces gastric acid secretion.
 Decreases gastric emptying.
 Stimulates the release of insulin.

Vasoactive Intestinal Peptide (VIP)

  Source
 Nerve fibers supplying all parts of the gastrointestinal tract.
 Triggers
 Unknown at this point.
 Actions
 May have various effects on many parts of the body, not only the gastrointestinal tract.
 Vasodilator – increases blood flow to the gut.
 Empties water and electrolytes into pancreatic enzymes and bile.
 May affect water and electrolyte transport between the bloodstream and gut lumen.
 Relaxes smooth muscle, particularly that of the sphincters.
 May play a role in blood glucose regulation.

Guanylin
 Source
 Small intestine.
 Colon
 Trigger
 Causes diarrhea which may be in response to certain stimuli (not as yet ascertained).
 Actions
 Secretion of chloride.
 Decreases absorption of water from the gut.

Glucose-dependent insulinotropic peptide

 Source
Glucose-dependent insulinotropic are produced by K cells in the upper small intestinal mucosa, gastric
antrum and ileum.
 Source
inhibits gastric secretions.

2. Skin

 When ultraviolet radiation strikes the skin, it triggers the conversion of dehydrocholesterol
(a cholesterol derivative) into calciferol (vitamin D3).
 Calciferol travels in the blood to the liver where it is converted into 25[OH] vitamin D 3.
 This compound travels to the kidneys where it is converted into calcitriol (1,25 [OH]2 vitamin D3). This
final step is promoted by the parathyroid hormone (PTH)

Although called a vitamin, calciferol and its products fully qualify as hormones because they are

 made in certain cells,

 carried in the blood,
 affect gene transcription in target cells.

3. Heart

Natriuretic Peptides (natrium = sodium; uresis = urinate)

In response to a rise in blood pressure, the heart releases two peptides:

 A-type Natriuretic Peptide (ANP):This hormone is released from stretched atria (hence the "A").
 B-type Natriuretic Peptide (BNP):This hormone is released from the ventricles. (It was first discovered
in brain tissue; hence the "B".)
Both hormones lower blood pressure by

 relaxing arterioles
 inhibiting the secretion of renin and aldosterone
 inhibiting the reabsorption of sodium ions by the kidneys.

The latter two effects reduce the reabsorption of water by the kidneys. So the volume of urine increases as does the
amount of sodium excreted in it. The net effect of these actions is to reduce blood pressure by reducing the volume
of blood in the circulatory system.

4. Kidney Hormones
Erythropoietin
Erythropoietin regulates erythropoiesis. In adults, approximately 90 % of erythropoietin is synthesized in the
kidneys (interstitial cells) , the remaining amount in the liver (perivenous hepatocytes) . The liver plays a key role in
the production of erythropoietin during the fetal period.

Calcitriol (1,25- dihydroxycholecalciferol)

Calcitriol stimulates the small intestine for protein synthesis allowing absorption of Ca2+and phosphates. This
ensures the availability of Ca2+ and phosphate for bone growth. Calcitriol simultaneously activates osteoblasts to
synthesize collagen.

3. Renin-Angiotensin-Aldosterone System: assists with this in the following manner:

1. The glomulerus, a bundle of capillary blood vessels found in the kidney, senses a drop in blood flow or
sodium and secretes an enzyme called renin into the bloodstream.
2. Renin moves to the liver where it converts the inactive peptide angiotensinogen to angiotensin I.
3. Angiotensin I travels to the lungs where another enzyme converts it to angiotensin II.
4. Angiotensin II
1. constricts the walls of arterioles closing down capillary beds;
2. stimulates the proximal tubules in the kidney to reabsorb sodium ions;
3. stimulates the adrenal cortex to release aldosterone. Aldosterone causes the kidneys to reclaim
still more sodium and thus water.
4. increases the strength of the heartbeat;
5. stimulates the pituitary to release the vasopressin .

All of these actions lead to an increase in blood pressure.