Effect of hypergastrinemia and blockade of gastrin-receptors on pancreatic growth in the mouse.

BACKGROUND/AIM: The present study evaluates whether endogenous gastrin regulates pancreatic growth in the mouse.

MATERIALS AND METHODS

Male NMRI mice weighing 12-15 g were assigned to six groups (10 mice/group) which were treated with different combinations of 0.9% NaCl, omeprazole, a CCK-A antagonist, a CCK-B antagonist, loxiglumide, and L365, 260 for 10 days each according to different protocols.

RESULTS

Omeprazole caused a marked, 10-fold increase in serum gastrin which was not affected by the gastrin antagonist, but markedly reduced by the CCK-A antagonist. The marked increase in endogenous gastrin caused by omeprazole did not promote pancreatic growth in any way. Similarly, the gastrin antagonist did not inhibit pancreatic growth. In contrast, the CCK-A antagonist significantly decreased pancreatic weight and protein content.

CONCLUSIONS

The present results strongly suggest that endogenous gastrin--in contrast to CCK--does not regulate pancreatic growth in the mouse. The inhibitory effect of loxiglumide on omeprazole-induced increase in serum gastrin might be explained by recent findings which showed that CCK-A antagonists can stimulate gastric acid secretion probably due to a reduction of the inhibitory effect of basal CCK on the D-cell and its somatostatin release. Probably such a slight stimulation of gastric acid secretion caused by the CCK-A antagonist might reduce the gastrin increase caused by omeprazole's abolishment of acid secretion.