Bombesin and G-17 dose responses in duodenal ulcer and controls

Hirschowitz, Basil I.; Tim, L. Ou; Helman, Colin A.; Molina, E

doi:10.1007/bf01315608

Cited by 36 publications

(13 citation statements)

References 24 publications

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“…4 B). Therefore, our results indicate that parietal cells of DU patients and normal controls have identical responsiveness (sensitivity) to circulating human G-17, a conclusion recently reached by Hirschowitz et al (5).…”

Section: Discussionsupporting

confidence: 67%

“…Studies by Isenberg, Lam, and their associates have suggested that parietal cells ofpatients with duodenal ulcer (DU)' are more responsive to gastrin than parietal cells of normal subjects (2,3). This is controversial, however, since acid secretory responsiveness to exogenous gastrin was similar in DU patients and controls studied by Hirschowitz et al (4,5). In the present study, we compared acid secretory responsiveness to human gastrin heptadecapeptide (G-17) in DU patients and controls.…”

Section: Introductionmentioning

confidence: 91%

See 1 more Smart Citation

Comparison of acid secretory responsiveness to gastrin heptadecapeptide and of gastrin heptadecapeptide pharmacokinetics in duodenal ulcer patients and normal subjects.

et al. 1986

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Serum gastrin concentrations and gastric acid secretion were measured during intravenous infusion of gastrin heptadecapeptide (G-17) (0, 7, 22.1, 70, 221, and 700 pmol/kg. h) in 15 duodenal ulcer patients and 15 healthy controls. Ulcer patients developed higher serum gastrin concentrations during G-17 infusion due to nearly twofold slower clearance of gastrin (8.8 vs. 15.7 ml/ kg-min; P < 0.01). Despite slower clearance of G-17, ulcer patients had plasma elimination half-times for G-17 similar to controls (6.0 vs. 6.1 min, respectively). Thus, calculated volume of distribution for G-17 was lower in ulcer patients than controls (78.5 vs. 140.7 ml/kg, P < 0.025). For any serum gastrin during gastrin-17 infusion, acid secretion (millimoles per hour) was higher in ulcer patients than in controls. However, when acid secretion was expressed as a percentage of peak acid output to G-17 (to correct for differences in parietal cell mass), curves relating acid secretion to serum gastrin were identical in ulcer patients and controls.

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Section: Discussionsupporting

confidence: 67%

Section: Introductionmentioning

confidence: 91%

Comparison of acid secretory responsiveness to gastrin heptadecapeptide and of gastrin heptadecapeptide pharmacokinetics in duodenal ulcer patients and normal subjects.

et al. 1986

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“…Bombesin-stimulated gastrin release is considerably greater in DU patients than in controls. 26 DU patients, also showed a different pattern of acid secretion in response to bombesin. Low doses produced similar acid secretion in DUs and controls.…”

Section: Somatostatin In Duodenal Ulcermentioning

confidence: 89%

Helicobacter pylori and gut hormones

Kaneko

Konagaya

Kusugami

2002

Journal of Gastroenterology

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Helicobacter pylori infection has been found to decrease the expression of antral somatostatin and to increase the release of the acid-stimulating hormone gastrin. The reversal of these changes in gut hormones by the eradication of H. pylori, and in-vivo and in-vitro studies in animals either infected with H. pylori or exposed to H. pylori-related materials may support the somatostatin-gastrin link theory in the pathophysiology of H. pylori infection. The following mechanisms have been proposed to explain the H. pylori infection-associated changes in gut hormones; (1) ammonia produced by H. pylori and monochloramine, (2) effect on somatostatin receptor subtype-2, (3) action of lipopolysaccharide from H. pylori on somatostatin receptor, (4) inflammatory cells and mediators, and (5) bacterial strain diversity. H. pylori infection can alter gastric acid secretion in both directions. The elevated acid secretion in patients with duodenal ulcer is decreased by H. pylori eradication, and is accompanied by the normalization of gut hormones in patients whose H. pylori-induced gastritis is limited to the antrum with hyperacidity. Corpus gastritis and the subsequent development of mucosal atrophy induced by H. pylori result in decreased acid secretion, although the mechanism underlying H. pylori-induced atrophy in some subjects remains unclear. Hypoacidity enhances corpus atrophy and increases gastrin secretion, mediated via a physiological suppression of somatostatin release, features that are also observed in H. pylori infection. Therefore, the capacity of acid secretion and distribution of gastritis or atrophy should be taken into consideration when we discuss the affect of H. pylori on gut hormones.

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“…Following on the elegant studies of bombesin-stimulated gastrin and acid secretion by Hirschowitz et al 33 , the group in Glasgow evaluated acid secretion stimulated by the human bombesin equivalent GRP. They showed that GRP-stimulated acid secretion was exaggerated in patients with duodenal ulcer compared with uninfected patients or those with H. pylori infection without duodenal ulcer disease.…”

Section: Secretionsmentioning

confidence: 99%