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
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.