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Gastric endocrine cells

Arnold R, Koop H, Schwarting H et al. (1986) Effect of acid inhibition on gastric endocrine cells. Scand J Gastroenterol 21 (Suppl 125) 14-19... [Pg.153]

Creutzfeldt W, Stockmann F, Conlon 1M et al. (1986) Effect of short- and long-term feeding of omeprazole on rat gastric endocrine cells. Digestion 35 (Suppl 1 ) 84—97 Ekman L, Hansson E, Havu N et al. (1985) Toxicological studies on omeprazole. Scand J Gastroenterol 20 (Suppl 108) 53-69... [Pg.153]

Thompson M, Fleming KA, Evans DJ, et al. Gastric endocrine cells share a clonal origin with other gut cell lineages. Development 1990 110 477-481. [Pg.226]

Sachs G, Zeng N, Prinz C (1997) Physiology of isolated gastric endocrine cells. Ann Rev Physiol 59 243-256... [Pg.44]

No large-scale surveillance reports are yet available for omeprazole or other PPIs. However, neither gastric carcinoids nor carcinomas have been observed in several prospective long-term studies for up to 10 years with omeprazole, nor has dysplasia of the gastric endocrine cells or the mucosa been found in multiple biopsies. Also, no increase in intestinal metaplasia occurred [14, 31, 35]. [Pg.106]

Borch K, Renvall H, Liedberg G (1985) Gastric endocrine cell hyperplasia and carcinoid tumors in pernicious anemia. Gastroenterology 88 638-648... [Pg.110]

Solcia E, Rindi G, Havu N, Elm G (1989) Qualitative studies of gastric endocrine cells in patients treated long-term with omeprazole. Scand J Gastroenterol 24(Suppl 166) 129-137... [Pg.111]

Lehy T, Mignon M, Cadiot G, Elouaer-Blanc L, Ruszniewski P, Lewin MJ, Bonfils S (1989) Gastric endocrine cell behavior in Zollinger-Ellison patients upon long-term potent antisecretory treatment. Gastroenterology 96 1029-1040... [Pg.218]

Hakanson R, Ekelund M, Sundler F (1984) Activation and proliferation of gastric endocrine cells. In S Falkmer, R Hakanson, F Sundler (eds) Evolution and tumor pathology of the neuroendocrine system. Elsevier, Amsterdam, 371-398... [Pg.220]

Lehy T, Cadiot G, Mignon M, Ruszniewski P, Bonfils S (1992) Influence of multiple endocrine neoplasia type 1 on gastric endocrine cells in patients with the Zollinger-Ellison syndrome. Gut 33 1275-1279... [Pg.222]

Lamberts R, Creutzfeldt W, Stockmann F, Jacubaschke U, Maas S, Brunner G (1988) Longterm omeprazole treatment in man effects on gastric endocrine cell populations. Digestion 39 126-135... [Pg.222]

Secretin Endocrine cells in mucosa of duodenum Acid in duodenum Inhibits gastric emptying and gastric secretion stimulates secretion of bicarbonate from pancreas stimulates secretion of bicarbonate-rich bile from liver... [Pg.284]

Gastric inhibitory Endocrine cells in mucosa Lipids, acid, and Inhibits gastric emptying and gastric... [Pg.284]

Gastrin is a hormone produced by gastric endocrine tissue — specifically, the G cells in the pyloric gland area. It is released into the blood and carried back to the stomach. The major function of gastrin is to enhance acid secretion by directly stimulating parietal cells (HC1) and chief cells (pepsinogen). Gastrin also stimulates the local release of histamine from enterochromaf-fin-like cells in the wall of the stomach. Histamine stimulates parietal cells to release HC1. [Pg.293]

Figure 4.1 Components of a gastric gland. The pit and the luminal surface are lined by surface mucous cells. The isthmus contains stem and progenitor cells and is enclosed by a sheath of myofibroblastic cells. Mucous neck cells are found in the neck, while chief and endocrine cells are present in the base of the gland. Parietal cells are actually scattered throughout the gland. Figure 4.1 Components of a gastric gland. The pit and the luminal surface are lined by surface mucous cells. The isthmus contains stem and progenitor cells and is enclosed by a sheath of myofibroblastic cells. Mucous neck cells are found in the neck, while chief and endocrine cells are present in the base of the gland. Parietal cells are actually scattered throughout the gland.
Gastric acid secretion can be inhibited by several mechanisms including acid in the stomach (pH 3 inhibits gastrin release), acid in the duodenum, the presence of fat in the pancreas, and hypertonic fluids or hyperglycemia. Somatostatin, a hormone produced by antral mucosal endocrine cells (D cells), inhibits the release of gastrin by directly inhibiting the parietal cells. Somatostatin is also present in other GI tissue and the pancreas. C cells, endocrine cells in the proximal small intestine, secrete secretin in response to mucosal acidification, which also decreases gastric secretion. [Pg.1223]

BIO. Borch, K., Renvall, H., Liedberg, G., and Andersen, B. N., Relations between circulating gastrin and endocrine cell proliferation in the atrophic gastric fundic mucosa. Scand. J. Gastroenterol. 21, 357-363 (1986). [Pg.258]

Pernicious anaemia. End stage of 10-15% of autoimmune gastritis due to vitamin B12 malabsorption caused by depletion of gastric parietal cells and autoantibodies against intrinsic factor. Associated with a variety of autoimmune endocrine diseases (e.g. -Hashimoto thyroiditis, Addison disease) and autoimmune myasthenic syndromes. [Pg.248]

Motilin is a 22-amino-acid polypeptide isolated by Brown et al. [2] in the search for duodenal factors stimulating gastric motility in dogs by intraduodenal alkalization. Although differences in the amino acid sequence among animal species are seen, the 6-amino-acid sequence of the N terminal is common to the species. Pearse et al. [3] reported that, using an indirect immunofluorescence technique, motilin is produced by a type of endocrine cell that is abundant in the duodenum and jejunum. [Pg.502]

Pancreatic polypeptide (PP) Endocrine cells in periphery of islets in the head of the pancreas 1. Reduces CCK-mediated gastric acid secretion 2. Increases intestinal transit time (slows motility) Stimulated by intraluminal nutrients, hypoglycemia, and vagal nerve stimulation... [Pg.801]

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