title: Lessons from the gastrin and gastrin receptor knockout mice.
abstract: The gastric hormone gastrin was first recognized for its ability to induce acid secretion. Following the purification and subsequent development of specific radioimmunoassays for gastrin, it was also shown to be a regulator of oxyntic mucosal growth. To examine the importance of gastrin or its receptors during development in general and for gastric physiology specifically both have been knocked out. Gastrin and gastrin receptor knockout mice are viable, develop without any gross abnormalities, and are fertile. Even though gastrin acts as a growth factor during hypergastrinemia there was no general atrophy of the gastric mucosa in the knockout mice. However, the maturation of both parietal and ECL cells was disturbed and the number of parietal cells was reduced. Basal acid secretion was impaired and rendered the parietal cells unresponsive to secretagogues. Outside the stomach the mice had no apparent phenotype. However, studies have suggested that progastrin and glycine-extended proforms of gastrin may have biological importance, but these results are still circumstantial and identification of the implicated receptors will be crucial for further studies.
authors.affiliation: Dept. of Clinical Biochemistry, Rigshospitalet, University of Copenhagen, Denmark. lfh01@bbh.hosp.dk
authors.forename: L
authors.initials: L
authors.lastname: Friis-Hansen
mesh_terms: D000818:Animals; D002766:Cholecystokinin / Q000172:deficiency / Q000235:genetics / Q000502:physiology; D015179:Colorectal Neoplasms / Q000209:etiology; D005753:Gastric Mucosa / Q000254:growth & development / Q000502:physiology; D005755:Gastrins / Q000172:deficiency* / Q000235:genetics* / Q000502:physiology; D015870:Gene Expression; D051379:Mice; D018345:Mice, Knockout; D010641:Phenotype; D011949:Receptors, Cholecystokinin / Q000172:deficiency* / Q000235:genetics* / Q000502:physiology
chemical_list: D005755:Gastrins; D011949:Receptors, Cholecystokinin; D002766:Cholecystokinin