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1. Pure ethanol does not stimulate gastrin release in humans.

2. To overcome this problem we have measured gastrin mediated acid secretion after the intravenous infusion of gastrin releasing peptide.

3. Future studies evaluating mechanisms of gastrin release have to take into account the H pylori state.

4. The role of the increased serum gastrin concentration induced by H pylori in the pathogenesis of duodenal ulcer disease is also unknown.

5. Similarly, basal serum gastrin concentrations do not alter with ageing in healthy men.

6. Carbachol, gastrin, and histamine all bind to specific receptors on parietal cell plasma membranes.

7. Our finding that fasting serum gastrin consists mainly of G34 is consistent with previous reports.

8. For gastric acid secretion, basal serum gastrin was considered in addition to these three variables.

9. They found that patients with the highest serum gastrin concentrations did not necessarily have the highest enterochromaffin like cell counts.

10. The potential autocrine grown effects of gastrin in colorectal cancer have previously been studied using cell lines.

11. The serum gastrin concentration was determined by radioimmunoassay using antibody R98.

12. Increased basal serum gastrin is related to both atrophy and H pylori infection but not to ageing perse.

13. There was no relationship between the serum gastrin concentration and type of renal replacement treatment.

14. This was also true when gastrin and intrinsic factor were incubated together with their respective antibodies.

15. The plasma gastrin concentrations increased from group to group as expected from the dose given.

16. The exaggerated acid response to gastrin can be explained by the increased parietal cell mass present in duodenal ulcer patients.

17. Serum gastrin concentrations did not correlate well with changes in the endocrine cell density.

18. Gastrin levels may also be elevated by pernicious anemia. duodenal ulcers, and after a meal.

19. Integrated meal stimulated serum gastrin outputs were determined by calculating the area under the serum concentration time curve.

20. H pylori has variable effects on serum gastrin concentrations and gastric acid secretion.

21. Helicobacter pylori increases plasma gastrin concentrations by 50% to 100% and values fall to normal after the organism has been eradicated.

22. The finding of enhanced fasting gastrin concentrations in H pylori positive subjects and in duodenal ulcer disease can not easily be explained.

23. Subjects with atrophy had significantly higher serum gastrin concentrations than all other subjects and higher than old subjects without atrophy.

24. There have been conflicting reports concerning the form of gastrin that is increased in H pylori infection.

25. Most investigators have observed that H pylori infection causes a greater percentage increase in the postprandial gastrin than fasting gastrin.

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26. Further characterisation of the non-ethanolic component of beer and wine that stimulates acid and gastrin secretion needs to be carried out.

27. We therefore also plotted individual dose-response curves of log plasma gastrin against the basal-subtracted acid output.

28. In another study by Ryberg etal the enterochromaffin like cell labelling index was shown to increase linearly with the plasma gastrin concentration.

29. Our finding also confirms previous reports that postprandial serum gastrin consists of approximately equivalent concentrations of G17 and G34.

30. It seems possible that this material originates from rare mucosal endocrine cells expressing the gastrin gene.