THE EFFECT OF GASTRIN-RELEASING PEPTIDE ON GASTRIN AND SOMATOSTATIN MESSENGER-RNAS IN HUMANS INFECTED WITH HELICOBACTER-PYLORI

Citation
Ah. Gibbons et al., THE EFFECT OF GASTRIN-RELEASING PEPTIDE ON GASTRIN AND SOMATOSTATIN MESSENGER-RNAS IN HUMANS INFECTED WITH HELICOBACTER-PYLORI, Gastroenterology, 112(6), 1997, pp. 1940-1947
Citations number
51
Categorie Soggetti
Gastroenterology & Hepatology
Journal title
ISSN journal
00165085
Volume
112
Issue
6
Year of publication
1997
Pages
1940 - 1947
Database
ISI
SICI code
0016-5085(1997)112:6<1940:TEOGPO>2.0.ZU;2-I
Abstract
Background & Aims: Gastrin-releasing peptide stimulates gastrin secret ion but also inhibits its release via somatostatin, Exogenous gastrin- releasing peptide stimulates a greater increase in plasma gastrin conc entrations in patients infected with Helicobacter pylori than in uninf ected controls, Because this infection suppressed gastric mucosal soma tostatin, we studied whether the increased gastrin response was a resu lt of an abnormal response of the somatostatin cell, Methods: Patients without dyspeptic ulcers received an infusion of either gastrin-relea sing peptide or saline on separate occasions. Acid secretion was measu red, and gastric biopsy specimens were taken for gastrin and somatosta tin messenger RNA (mRNA) analysis and H. pylori diagnosis, Results: In response to gastrin-releasing peptide, the increase in plasma gastrin concentrations in the infected patients was significantly higher than in the uninfected, Antral gastrin mRNA also increased significantly i n the infected group but decreased significantly in the uninfected gro up, Basal somatostatin was lower in the infected group; gastrin-releas ing peptide produced a significant increase in antral somatostatin mRN A concentration in infected, but not uninfected, patients, Conclusions : The somatostatin cell responds to gastrin-releasing peptide in H. py lori infection, Gastrin-releasing peptide normally inhibits gastrin mR NA expression, but inhibition is deficient in H. pylori infection, pos sibly because of low stimulated somatostatin levels.