The precursor of gastrin ‘preprogastrin’ can be converted into several types of gastrin hormones, namely, G-34, G-17, and G-14, depending on the number of amino acid that are attached. The carboxyl terminal tetrapepetide contain more than 45 amino acids residues attached. The tryptophan present in the 6th amino acid may be sulfated or non-sulfated. Both non-sulfated and sulfated types of gastrin are present in the blood in equal amounts (Ganong, 2005). Different types of gastrin produce different actions in the body. One of the forms that are present in the largest quantities in the body is G-17.
The half-life of G-34 is 15 minutes, and that of G-14 and G-17 is about 2 to 3 minutes. Enzymes present in the small intestines and the kidneys help to inactivate the gastrin (Ganong, 2005). Gastrin secretion may be increased or decreased by several factors. These include local, neuronal and hematological factors. Gastrin secretion increased due to distention of the stomach, presence of amino acids or peptides in the diet (such has phenylalanine and tryptophan), increase in vagal discharge, calcium channel, adrenaline, etc.
The secretion is decreased due to somatostatin secretion, GIP, VIP, glucagon, calcitonin, acid secretion, etc (Ganong, 2005). Gastrin has several important functions and activities in the GIT. These includes increased secretion of the gastric acid and pepsin secretion, encouragement of growth and development of the mucosa of the gastric lining, small intestines and large intestines, encouragement of the smooth muscles movement of the stomach, increase in the insulin release controlling protein metabolism and non-carbohydrates metabolism, etc.
In other parts of the body, such as the CNS, etc, gastrin is also secreted, but the role it plays is not understood clearly (Ganong, 2005). Gastrin usually binds to the receptor site present on the parietal cells. Several other substances such as acetylcholine and histamine also bind to these sites, thus encouraging the cell to release acids. The enterochromaffin cells also contain gastrin receptors, and it is being felt recently that gastrin secretion primarily act on these cells.
When the enterochromaffin cells are stimulated by gastrin secretion, histamine is released, which in turn binds to the H2 Receptors present in the parietal cells causing release of acid (Bowen, 2003). The manner in which gastrin secretion causes growth and development of the gastric mucosa has not been understood clearly. However, studies have suggested that the DNA, RNA and the protein synthesis activity rises, causing an increase in the number of parietal cells. This may be proved by the fact individuals suffering from hypergastrinemia are at a higher risk of developing hypertrophy of the gastric mucosa (Bowen, 2003).