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Hildebrand et al reported data suggesting that gastrin releasing peptide (GRP) may be a physiological regulator of pre- and postprandial gastric acid secretion (Gut 2001;49:23–8). Interestingly, these effects were independent of gastrin and the authors appropriately questioned the physiological role of gastrin in regulating gastric secretion. Several aspects of the authors' conclusions deserve further clarification and discussion.
The authors concluded that alteration of somatostatin secretion is unlikely to explain the acid inhibitory action of BIM26226 because the GRP antagonist did not alter somatostatin mRNA levels. They also argued that the lack of change of gastrin mRNA supported the physiological data showing no alteration in gastrin secretion with BIM26226. In short term experiments such as these, it is incorrect to …