More than 30 peptide hormone genes are known to be expressed throughout the digestive tract, which makes the gut the largest endocrine organ in the body. These hormones may act in an endocrine (enter the bloodstream and act at sites distant from the site of secretion), paracrine (act locally) , autocrine (act on self) or neurocrine (produced by GIT neurons) fashion. Many GIT hormones enter the portal circulation first before reaching the systemic circulation which takes them to their target organ.
Neurocrines are secreted by enterochromaffin cells of the GIT. Acetylcholine, norepinephrine, VIP, GRP, enkephalins, neuropeptide Y and substance P are the GIT neurocrines. Some neurocrines act as neuromodulators i.e. they modulate the activity of neurotransmitters. ACh causes contraction of smooth muscle in the wall and relaxation of sphincters (makes you go) and increases all GIT secretions. Norepinephrine causes relaxation of smooth muscle in the wall (flight and fright hormone, makes you hold) and contraction of sphincters. Galanin is a newly discovered neuromodulator that affects GIT motility and secretions. It is predominantly inhibitory and acts through G-protein coupled receptors.
Hormone | Stimuli for secretion | Effect |
Gastrin* | Peptides and amino acids especially tryptophan and phenylalanine; distension of stomach; GRP | Increased gastric acid secretion by parietal cells; stimulates growth of gastric and intestinal mucosa |
CCK or cholecystokinin | Peptides, amino acids, monoglycerides | Increased pancreatic enzyme and HCO3- secretion; contraction of gallbladder and relaxation of the sphincter of Oddi; slows gastric emptying; stimulates growth of exocrine pancreas and gallbladder |
Secretin** | H+ and fatty acids | Increased pancreatic HCO3- secretion;decreased gastric acid secretion; inhibits gastrin |
Motilin | Released by enterochromaffin cells in fasting | Increases GIT motility by stimulating the migratory motor complexes. |
GIP or glucose dependent insulinotropic peptide or gastric inhibitory peptide | Oral glucose, amino acids and fatty acids | Increased secretion of Insulin; decreased gastric H+ secretion; satiety; slows gastric emptying |
GLP 1 or glucagon like peptide 1 | Hexoses and fat | Decreases gastric emptying; satiety; increases sensitivity of beta cells of the pancreas to glucose; inhibits glucagon secretion; lowers blood glucose levels; |
Enteroglucagon | Low blood glucose | Stimulates glycogenolysis and gluconeogenesis in the liver. |
Pancreatic polypeptide | Ingestion of a meal | Inhibits pancreatic secretion of HCO3-; satiety |
Somatostatin | Decreased luminal pH | Inhibits other GIT hormones and inhibits H+ secretion |
Histamine | Gastrin | Stimulates H+ secretion by gastric parietal cells |
VIP or vasoactive intestinal peptide | Enterochromaffin cell stimulation | Relaxation of smooth muscle in GIT; increased intestinal and pancreatic secretion; |
GRP or gastrin releasing peptide or Bombesin | Enterochromaffin cell stimulation | Increases secretion of gastrin |
Enkephalins (opiates) | Enterochromaffin cell stimulation | Smooth muscle contraction; decreased secretion |
Substance P | Enterochromaffin cell stimulation | Contraction of smooth muscle; increased secretion of saliva |
Neuropeptide Y | Enterochromaffin cell stimulation | Relaxation of smooth muscle; decreased intestinal secretion |
Serotonin | Enterochromaffin cell stimulation | Inhibits gastric acid secretion; stimulates gastric and colonic mucus production; modulates GI smooth muscle activity and blood flow |
Ghrelin | Fasting; vagal stimulation | Stimulation of appetite; increases food intake; modulates gastric acid secretion and motility; modulates pancreatic endocrine and exocrine secretions; increases GH secretion. |
*Gastrin levels will increase in Zollinger-Ellison syndrome, H.pylori infections and chronic use of H2 blockers and proton pump inhibitors.
**Action of secretin is important as pancreatic lipases are active only at alkaline pH.
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