Mechanism of gastrin secretion in duodenal ulcer in response to insulin induced hypoglycemia
Ferraù, O.; Familiari, L.; Turiano, S.; Consolo, F.
Bollettino della Societa Italiana di Biologia Sperimentale 51(8): 455-460
1975
ISSN/ISBN: 0037-8771 PMID: 1212333 Document Number: 83023
Attention is called to the conflicting reports on the role of gastrin secretion in the development of human duodenal ulcer. The theory that because of excessive gastric acid secretion by the stomach, common in peptic ulcer patients, there may be hyperplasia of gastrin (G) cells, is discussed. The high gastric acid content would them feed back, causing blood gastrin to fall. Experiments were performed based on the stimulation on gastrin secretion produced by insulin hypoglycemia. Removal of stomach acid by neutralization supposedly stops the inhibition exercised by acid secretion on gastrin secretion. Conflicting results of these previous experiments led to the use of a new experimental design in which gastric acid was removed by suction and not by neutralization. Experiments on 10 normal subjects and on 13 with known duodenal ulcer in which blood samples were taken before and after insulin administration, and assayed for gastrin content at 15 min intervals for 2 h, were performed. The gastrinemia curves of normals showed a peak which came earlier and was slightly higher than that of ulcer patients. The significance of these findings is uncertain. Individual physiological situations in duodenal ulcer patients may increase gastrin response.