Gastrin as a growth factor in the gastrointestinal tract

The peptide hormone gastrin, released from antral G cells, is known to stim ulate the synthesis and release of histamine from ECL cells in the oxyntic mocosa via CCK-2 receptors. The mobilized histamine induces acid secretion by binding to the H-2 receptors located on parietal cells. Recent studies s uggest that gastrin, in both its fully amidated and less processed forms (p rogastrin and glycine-extended gastrin), is also a growth factor for the ga strointestinal tract. In this article, we review the recent evidence (inclu ding those from the transgenic and knockout mice) for the trophic targets o f both the amidated and less processed forms of gastrin in the gastrointest inal tract, pancreas and liver. It has been established that the major trop hic effect of amidated gastrin is for the oxyntic mucosa of stomach, where it causes increased proliferation of gastric stem cells and ECL cells, resu lting in increased parietal and ECL cell mass. There is insufficient eviden ce to support that amidated gastrin is a trophic factor for the rest of gas trointestinal tract, exocrine pancreas and liver. On the other hand, the ma jor trophic target of the less processed gastrin (e.g. glycine-extended gas trin) appears to be the colonic mucosa. There is no evidence to suggest tha t it is trophic for the stomach. It remains to be examined whether the rest of gastrointestinal tract, pancreas and liver are the trophic targets by g lycine-extended gastrin and progastrin. (C) 2000 Elsevier Science B.V. All rights reserved.