GI Hormones by dr anita teli

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Gastrointestinal hormones:

Gastrointestinal hormones Dr Anita.Teli

Introduction :

Introduction The word hormone derived from greek word ‘Hormaein’ means to execute or to arouse or to act in motion, was coined by W.B.Hardy for such substances which circulate in the blood & bring about an effect on a distant organ. Hormone was used by starling in 1905 to describe secretin & gastrin & to convey the concept of blood borne chemical messengers.

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Starling & Bayliss have defiened a hormone as a chemical agent which is released from one group of cells & travel via the blood stream to affect one or more different groups of cells. Huxley in 1935 has defiened hormones as information transfering molecules, the essential function of which is to transfer information from one set of cells to another for the good of the cell population as a whole.


GIT is the largest endocrine organ in the body. Its hormones were the first to be discovered. Released from the mucosa of stomach & small intestine. pass from portal circulation into general circulation & then to target tissue.

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Glandular cells secreting the hormones are dispersed as single cells among gastro intestinal mucosal cells. Hormone containing granules are concentrated at the base of the cells close to the capillaries. Cells called APUD cells . Origin – neural crest .

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Hormones released by Nervous activity Distension Chemical stimulation coincident with intake of food.

Discovery :

Discovery Four steps are required to establish the existence of a GI hormone . A physiologic event such as a meal must be demonstrated to provide the stimulus to one part of digestive tract that subsequently alters the activity in another part Effect must persist after all nervous connections between 2 parts of the tract have been severed.

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3) From the site of application of stimulation a substance must be isolated that when injected into blood , mimics the effect of stimulus. 4) The substance must be identified chemically & its structure must be confirmed by synthesis. Five GI peptides have achieved full status as hormones : secretin, gastrin, cholecystokinin, gastric inhibitory peptide, motilin.

Candidate hormones:

Candidate hormones Hormones whose significance has not been established Include several chemically defined peptides that have significant actions but whose hormonal status has not been proved. E.g. pancreatic polypeptide , neurotensin, substance P.

Classification :

Classification Gastrin family – gastrin & CCK Secretin family – GIP, Glucagon, Secretin, VIP, Glycentin. Others –motilin, neurotensin, bombesin, substance P, neuropeptide y, somatostatin, pancreatic polypeptide, guanylin, gastrin releasing peptide, chymodenin.

Gastrin :

Gastrin G-cells in antral & duodenal mucosa. Flask shaped cells with broad base & narrow apex. Microvilli from the apex of the cell into lumen. Receptors on the microvilli- detect changes in the gastric contents.

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Depending upon the no of AA : Little gastrin: G 17 90% 0f antral gastrin . More active. Big gastrin G 34 –this form seen after meal. Not as active as little form. Mini gastrin-G 14 less active Big big gastrin-contains more than 34 AA. During interdigestive state. All the biologic activity of gastrin can be reproduced by the 4 C-terminal AA.

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After meal antral gastrin G 17 is released & provides most of the stimulus for acid secretion. Half life : G 14 , G 17 - 2 -3 min G 34 – 15 min. Inactivated primarily in the kidney & small intestine.

Also found :

Also found Pancreatic islets in fetal life. Anterior & intermediate lobes of pituitary, hypothalamus & medulla oblongata. Vagus & sciatic nerves.

Stimulus :

Stimulus Sight, smell, taste of food vagal output Gastrin release ( cephalic phase) Gastric distension & presence of nutrients Gastrin release.( gastric phase) Duodenal distension gastrin secretion from duodenal G cells( intestinal phase)

Stimuli increasing gastrin secretion:

Stimuli increasing gastrin secretion Luminal - peptides & amino acids (phenylalanine & tryptophan) - distension Neural - increased vagal discharge via GRP Blood borne - calcium - epineprine

Stimuli that inhibit:

Stimuli that inhibit Luminal –acid, somatostatin Blood borne - secretin, GIP, VIP, glucagon, calcitonin.

Actions :

Actions Stimulation of gastric acid & pepsin secretion Stimulation of growth of mucosa of stomach, small intestine & large intestine (trophic action) Stimulation of gastric motility. Stimulates insulin secretion after protein meal. Contraction of gastro esophageal sphincter.

Actions (contd):

Actions (contd) 6 . Stimulates pancreatic secretion. 7 . Increases antral motility but prolongs gastric emptying. 8 . Stimulates release of calcitonin which in turn inhibits gastrin secretion.

Clinical applications:

Clinical applications Gastrinoma( Zollinger Ellison syndrome) Non beta cell tumors of pancreas, duodenum. Produce gastrin at a high spontaneous rate, not altered by feeding. Hypergastrinemia hyper secretion of gastric acid by 2 mechanisms: 1 Trophic action of gastrin increased parietal cell mass & acid secretory capacity. 2 Increased serum gastrin stimulate secretion from the hyperplastic mucosa.

Cholecystokinin - Pancreozymin:

Cholecystokinin - Pancreozymin It is a polypeptide I cells upper small intestine. Acid, peptides, amino acids & fatty acids containing more than 10 carbon atoms in the duodenum stimulate. Half life- 5 min.

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Types CCK-58 found in brain CCK-39 CCK-33 CCk-12 in duodenum & jejunum. CCK-8 -do- CCK-4 enteric & pancreatic nerves

Functions :

Functions Contraction of gall bladder. Relaxes sphincter of oddi. Secretion of pancreatic juice rich in enzymes. Augments the action of secretin. Inhibits gastric emptying. Trophic effect on pancreas. Increases secretion of enterokinase. May enhance the motility of SI & colon. Along with secretin augments contraction of pyloric sphincter. CCK & gastrin stimulate release of glucagon.

Regulation of secretion.:

Regulation of secretion. Positive feed back mechanism. Terminated when products of digestion move on to the lower portions of GIT.


Other sites Found in nerves in distal ileum & colon. Brain – cerebral cortex. Two CCK receptors are identified 1. CCK-A located in the periphery & brain. 2. CCK-B located in the brain. Action – both activate PLC, increasing production of IP3 & DAG.

Secretin :

Secretin First hormone to be discovered by Starling & Bayliss in 1902. Secreted by S cells of upper small intestine. Half life- 5 min. 27 AA , all are required for activity.

Stimulus for secretion.:

Stimulus for secretion. Low pH [ <4.5] Products of protein digestion.

Functions :

Functions Secretion of bicarbonate & thus causes the secretion of a watery , alkaline pancreatic juice. Stimulates hepatic bile secretion. Augments the action of CCK. Decreases gastric acid secretion & causes contraction of pyloric sphincter. Inhibits gastric motility. Stimulate insulin secretion. Stimulates small intestinal secretion.

Regulation :

Regulation secretion stops - Once all the acid has been neutralized.

Gastric inhibitory peptide (GIP):

Gastric inhibitory peptide (GIP) K cells in the duodenum & jejunum. 42 aa. Secretion is stimulated by glucose & fat in the duodenum.

Functions :

Functions In large doses inhibits gastric secretion & motility, hence the name. Stimulates insulin secretion to get ready for glucose that is about to be absorbed (glucose dependent insulinotrophic hormone)

Vasoactive intestinal polypeptide (VIP):

Vasoactive intestinal polypeptide (VIP) Found in the nerves in the GIT Contains 28 aa. Half life 2 min in blood. Also found in brain & many autonomic nerves.

Actions :

Actions Stimulates intestinal secretion of electrolytes & water. Relaxation of intestinal smooth muscle including sphincters. Dilatation of peripheral blood vessels. Inhibits gastric acid secretion. Stimulates pancreatic secretion of both enzymes & bicarbonate.

Disorder :

Disorder Verner - Morrison syndrome [pancreatic cholera.] This is associated with VIPoma a type of VIP secreting tumors.( pancreatic islet cell tumor) Copious diarrhea bcoz of excess secretion of fluid & electrolytes.

Motilin :

Motilin 22 aa Secreted by enterochromaffin cells & Mo cells in stomach, small intestine, colon. Acts on G-coupled receptors on enteric neurons in duodenum & colon.

Functions :

Functions Stimulates stomach & intestinal motility during interdigestive phase & helps in clearing the food residue from previous meal. Its circulating level increases every 100 min in interdigestive state . Major regulator of migrating myoelectrical complex.

Applied :

Applied The antibiotic erythromycin binds to motilin receptors, & derivatives of this compound may be of value in treating patients in whom gastrointestinal motility is decreased.

Somatostatin :

Somatostatin D cells in gastric antrum, near gastrin secreting G cells or parietal cells. It exists in tissues in two forms: somatostatin 14 & 28. Stimulus – low pH in stomach, sympathetic stimulation.

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Inhibits acid secretion from parietal cells in 2 ways. Directly by its action on parietal cells. Indirectly by inhibiting release of gastrin. Inhibits the secretion of VIP, GIP, secretin & motilin. Also inhibits pancreatic exocrine secretion, gastric motility, gall bladder contraction & the absorption of glucose, amino acids & triglycerides.

Peptide YY:

Peptide YY 36 aa Secreted by small intestine & colon Release stmulated by fat. Inhibits gastric acid secretion & motility Decreases food intake.

Ghrelin :

Ghrelin 28 aa polypeptide Secreted primarily in stomach. Increases food intake Blood levels are reduced in fed state & increased during fasting.

Other GI hormones:

Other GI hormones 1) Neurotensin 13 aa Produced by neurons & cells that are abundant in the mucosa of ileum. Release stimulated by fatty acids. Inhibits gastrointestinal motility Increases ileal blood flow. 2) Substance P Endocrinal & nerve cells in GIT Increases the motility of small intestine.

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3) Enteroglucagon: L cells of intestine. 30 aa Potent insulin releaser Inhibits gastric secretion & emptying. 4) GRP 27 aa Present in vagal nerve endings that terminate on G cells Increases gastric acid secretion.

References :

References Johnson R Leonard. Regulation :peptides of GIT. Gastrointestinal physiology. 6 th edition. Mosby ; 2001. Pg 2-13. Khurana Indu. Text Book Of Medical Physiology. 1 st Edition, Elsevier; 2006. Pg 601, 619. Ganong W F. gastrointestinal hormones. Review of medical physiology.21 st edition .McGraw hill; 2003. Pg 486. Text book of physiology- A.K.Jain

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