Gastrin as a growth factor in the gastrointestinal tract

The peptide hormone gastrin, released from antral G cells, is known to stimulate the synthesis and release of histamine from ECL cells in the oxyntic mucosa via CCK-2 receptors. The mobilized histamine induces acid secretion by binding to the H(2) receptors located on parietal cells. Recent studies suggest that gastrin, in both its fully amidated and less processed forms (progastrin and glycine-extended gastrin), is also a growth factor for the gastrointestinal tract. In this article, we review the recent evidence (including those from the transgenic and knockout mice) for the trophic targets of both the amidated and less processed forms of gastrin in the gastrointestinal tract, pancreas and liver. It has been established that the major trophic effect of amidated gastrin is for the oxyntic mucosa of stomach, where it causes increased proliferation of gastric stem cells and ECL cells, resulting in increased parietal and ECL cell mass. There is insufficient evidence to support that amidated gastrin is a trophic factor for the rest of gastrointestinal tract, exocrine pancreas and liver. On the other hand, the major trophic target of the less processed gastrin (e.g. glycine-extended gastrin) appears to be the colonic mucosa. There is no evidence to suggest that 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 glycine-extended gastrin and progastrin.