Gastric acid secretion cholecystokinin

There are a variety of peptide hormones acting in the gut the gastrins stimulate gastric acid secretion secretin and somatostatin inhibit the production of gastrins. Cholecystokinin and somatostatin can inhibit gastric acid secretion directly, and the former one causes the gall-bladder to contract and thus force bile into the duodenum. 

Gastrin and cholecystokinin receptor ligands consisting of lH-imidazole-4-yl-benzooxazole derivatives, (II), prepared by Kalindjian (3) were effective in controlling excess gastric acid secretion. 

The duodenum releases secretin, which is a hormone that suppresses gastric acid secretion. This results in the intestinal juices having a higher pH than the gastric juices in the stomach. The hormone cholecystokinin is also released. It simulates the flow of bile into the duodenum. Hormones, bile, and pancreatic enzymes tr5 sin, chymotrypsin, lipase, and amylase digest carbohydrates, protein, and fat in preparation for absorption in the small intestine. 

Kanagawa K, Nakamura H, Murata, et al. Increased gastric acid secretion in cholecystokinin-1 receptor-deficient Otsuka Long-Evans Tokushima fatty rats. Scand J Gastroenterol 2002 37(1) 9-16. 

Pancreatic enemies (B) from slaughtered animals are used to relieve excretory insufficiency of the pancreas ( disrupted digestion of fats steatorrhea, inter alia). Normally, secretion of pancreatic enzymes is activated by cholecystokinin ancreozymin, the en-terohormone that is released into blood from the duodenal mucosa upon contact with chyme. With oral administration of pancreatic enzymes, allowance must be made for their partial inactivation by gastric acid (the lipases, particularly). Therefore, they are administered in acid-resistant dosage forms. 

Schematic diagram of one model of the physiologic control of hydrogen ion secretion by the gastric parietal cell. ECL cell, enterochromaffin-like cell G(CCK-B), gastrin-cholecystokinin-B receptor H, histamine H2, histamine H2 receptor Mi, M3, muscarinic receptors ST2, somatostatin2 receptor ATPase, K /H ATPase proton pump. Some investigators place histamine receptors—and possibly cholinoceptors—on nearby tissue cells rather than on the parietal cell itself. (Modified and redrawn from Sachs G, Prinz C Gastric enterochromaffin-like cells and the regulation of acid secretion. News Physiol Sci 1996 11 57, and other sources.)...

Gastric acid production is regulated by both the autonomic nervous system and several hormones. The parasympathetic nervous system, via the vagus nerve and the hormone gastrin, stimulates the parietal cell to produce gastric acid, acting both directly on parietal cells and indirectly through the stimulation of the secretion of the hormone histamine from ECL cells. Vasoactive intestinal peptides, cholecystokinin and secretin all inhibit acid production. 

Katschinski et al 1995). High doses of bethanechol increase release of gastrin, cholecystokinin and pemcreatic polypeptide. Unlike in other species, bethanechol does not increase gastric acid output in horses (Sandin et al 2000), but it does cause a small but significant increase in gastric fluid collection in cannulated horses (Thompson et al 1994), perhaps reflecting non-parietal secretions derived from the pancreas. 

Experiments performed in the 1920s and already described showed that acid and food, in particular fat, in the duodenum inhibit gastric secretion. Lim and his collaborator Kosaka made an extract of the duodenal mucosa that, upon intravenous injection into a dog, inhibited food-stimulated acid secretion, and they called the active component of their extract enterogastrone. Kosaka and Lim demonstrated that their extract did not stimulate pancreatic or biliary secretion and therefore did not contain secretin or cholecystokinin. In the 1960s, when it was possible to isolate purer and more potent compounds from the duodenal mucosa, R. A, Gregory extended the definition of enterogastrone to include inhibitors released from the intestine by acid and hypertonic solutions as well as by fat. " ... 

The long-chain fatty acids stimulate the secretion of cholecystokinin, which increases secretion of gastric lipase (i.e. positive feedback). 

In addition to the decreased intestinal absorption of calcium in uremia, calcium ATPase activity is also low (S6). Many gastrointestinal hormones are found in increased concentrations in uremia. These include gastrin (OlO), cholecystokinin (OlO), pepsinogen I (II), gastric inhibitory peptide (LI), amylase, and trypsin (R17). There is a decrease in the conjugation of cholic to deoxycholic acid (G13) and in the pancreatic secretion of bicarbonate (Oil). Hepatic output of urea is decreased, as is the activity of some urea cycle enzymes e.g., ornithine tran-scarbamylase (T9). The clinical significance of these hormonal and enzymatic perturbations remains to be elucidated. 

Gastric inhibitory peptide, GIF a polypeptide hormone (for structure, see Secretin) purified from crude preparations of Cholecystokinin (see). GIF has potent enterogastrone activity, i.e. it inhibits secretion of acid and pepsin by the stomach, and inhibits gastric motility. It possesses no significant secretin or cholecystokinin activity, [J.C. Brown J.R.Drybuigh Canad. J. Biochem. 49 (1971) 867-872]... 

---