dc.contributor.author | Waldum, Helge | |
dc.contributor.author | Sørdal, Øystein Finset | |
dc.contributor.author | Mjønes, Patricia | |
dc.date.accessioned | 2019-09-24T09:18:34Z | |
dc.date.available | 2019-09-24T09:18:34Z | |
dc.date.created | 2019-06-20T14:38:22Z | |
dc.date.issued | 2019 | |
dc.identifier.citation | International Journal of Molecular Sciences. 2019, 20:2444 (10), 1-11. | nb_NO |
dc.identifier.issn | 1422-0067 | |
dc.identifier.uri | http://hdl.handle.net/11250/2618416 | |
dc.description.abstract | Background: Studies on the regulation of gastric and pancreatic secretion began more than 100 years ago. Secretin was the first hormone postulated to exist, initiating the field of endocrinology. Gastrin produced in the antral mucosa was the second postulated hormone, and together with histamine and acetylcholine, represent the three major gastric acid secretagogues known since 1920. For a long time, the mast cell was the only recognized histamine-producing cell in the oxyntic mucosa and, in the mid-1980s, the ECL cell was recognized as the cell producing histamine, taking part in the regulation of gastric acid secretion. Methods: This review is based upon literature research and personal knowledge. Results: The ECL cell carries the gastrin receptor, and gastrin regulates its function (histamine release) as well as proliferation. Long-term hypergastrinemia results in gastric neoplasia of variable malignancies, implying that gastric hypoacidity resulting in increased gastrin release will induce gastric neoplasia, including gastric cancer. Conclusions: The trophic effect of gastrin on the ECL cell has implications to the treatment with inhibitors of acid secretion. | nb_NO |
dc.language.iso | eng | nb_NO |
dc.publisher | MDPI | nb_NO |
dc.rights | Navngivelse 4.0 Internasjonal | * |
dc.rights.uri | http://creativecommons.org/licenses/by/4.0/deed.no | * |
dc.title | The enterochromaffin-like [ECL] cell-central in gastric physiology and pathology | nb_NO |
dc.type | Journal article | nb_NO |
dc.type | Peer reviewed | nb_NO |
dc.description.version | publishedVersion | nb_NO |
dc.source.pagenumber | 1-11 | nb_NO |
dc.source.volume | 20:2444 | nb_NO |
dc.source.journal | International Journal of Molecular Sciences | nb_NO |
dc.source.issue | 10 | nb_NO |
dc.identifier.doi | 10.3390/ijms20102444 | |
dc.identifier.cristin | 1706505 | |
dc.description.localcode | © 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). | nb_NO |
cristin.unitcode | 194,65,15,0 | |
cristin.unitcode | 1920,15,0,0 | |
cristin.unitcode | 1920,14,0,0 | |
cristin.unitname | Institutt for klinisk og molekylær medisin | |
cristin.unitname | Medisinsk klinikk | |
cristin.unitname | Laboratoriemedisinsk klinikk | |
cristin.ispublished | true | |
cristin.fulltext | original | |
cristin.qualitycode | 1 | |