Transepithelial transducing cells, particularly the gastrin (G) cell, co-or
dinate gastric acid secretion with the arrival of food in the stomach. Rece
nt work suggests that multiple active products are generated from the gastr
in precursor, and that there are multiple control points in gastrin biosynt
hesis. Biosynthetic precursors and intermediates (progastrin and Gly gastri
ns) are putative growth factors; their products, the amidated gastrins, reg
ulate epithelial cell proliferation, the differentiation of acid-producing
parietal cells and histamine-secreting enterochromaffin-like (ECL) cells, a
nd the expression of genes associated with histamine synthesis and storage
in ECL cells, as well as acutely stimulating acid secretion. Gastrin also s
timulates the production of members of the epidermal growth factor (EGF) fa
mily, which in turn inhibit parietal cell function but stimulate the growth
of surface epithelial cells. Plasma gastrin concentrations are elevated in
subjects with Helicobacter pylori, who are known to have increased risk of
duodenal ulcer disease and gastric cancer. Studies of the physiology of ga
strin may therefore contribute to an understanding of the mechanisms releva
nt to major upper gastrointestinal tract disease.