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Carboxyl terminal glycine extended progastrin (gastrin‐G) in gastric antral mucosa of patients with gastric or duodenal ulcer and in gastrinomas
Author(s) -
AZUMA TAKESHI,
MAGAMI YASUSHI,
HABU YASUKI,
KAWAI KEIICHI,
TAGGART R. THOMAS,
WALSH JOHN H.
Publication year - 1990
Publication title -
journal of gastroenterology and hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.214
H-Index - 130
eISSN - 1440-1746
pISSN - 0815-9319
DOI - 10.1111/j.1440-1746.1990.tb01435.x
Subject(s) - gastrin , gastrinoma , antrum , medicine , g cell , gastroenterology , endocrinology , gastric mucosa , gastric acid , enterochromaffin like cell , stomach , secretion
Recently, carboxyl terminal glycine extended progastrin (gastrin‐G), the immediate biosynthetic precursor of amidated gastrin, was found in human gastric antral mucosa. To investigate the nature of gastrin amidation in pathophysiological conditions, we examined gastrin and gastrin‐G levels and their molecular forms in gastric antral mucosa of healthy controls and patients with gastric or duodenal ulcer and in gastrinomas. There were no significant differences between controls and gastric or duodenal ulcer patients in antral gastrin and gastrin‐G levels, the ratio of gastrin‐G to gastrin and the pattern of their molecular forms. In contrast, gastrin and gastrin‐G levels and the ratio of gastrin‐G to gastrin in gastrinomas were much higher than those in antral mucosa of controls or ulcer patients. The predominant molecular form of gastrin‐G was different between two Zollinger‐Ellison syndrome (ZES) cases. These results suggest that there are no significant differences between healthy controls and patients with gastric or duodenal ulcer in the nature of gastrin amidation, and that the nature of gastrin amination in gastrinomas is different from that in normal gastrointestinal tissues.