Abstract
In recent years, the gastrointestinal hormones gastrin and cholecystokinin-pancreo-zymin (CCK-PZ) have been looked upon as potential growth factors of the digestive tract glands. A survey on the spectrum of growth-related responses affected by these hormones shows that chronic in vivo administration of large amounts of pentagastrin produces oxyntic gland hyperplasia (1). Lichtenberger and Johnson (2) conclude from their studies on the ontogenic development of the small intestine, that some aspects are dependant on weaning and gastrin may be the mediator.
The hormonal control of pancreatic growth could be controlled by gastrin and CCK-PZ. Indeed, in hypophysectomized rats, pentagastrin treatment stimulates pancreatic hyperplasia in addition to hypertrophy (3). In normal rats, large doses of pentagastrin also result in pancreatic acinar cell hypertrophy (4).
Since CCK-PZ and gastrin share the same five C-terminal amino acids which comprise the active center of the gastrin molecule, one would thus expect the duodenal hormone to have comparable trophic effects on the pancreatic tissue. Recent data from Johnson and Guthrie (5) indicate a certain specificity of the trophic effect of CCK-PZ for the pancreatic tissue since CCK-PZ octa-peptide administration was associated with increases in DNA synthesis in the pancreas but not in the oxyntic gland or duodenum. Mainz et al. (6) established clearly that CCK-PZ administration at a dose of 20 IVY units kg, ip twice daily for 5 days, was associated with increases in cell mass and cell numbers. In similar studies, Barrowman and Mayston (7) also established the trophic effect of CCK-PZ on the exocrine pancreas.
Since the trophic effect of an hormone implies the regulation of a number of growth-related processes in the target tissue, such as stimulation of protein, RNA, and DNA synthesis, these major effects should be seen at any time during the normal growth of an animal.
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