ENDOGENOUS SOMATOSTATIN POSSIBLY CONTROLS PANCREATIC GROWTH - FURTHEREVIDENCE FOR FEEDBACK-REGULATION

Specific inhibitors acting upon pancreatic proteinases in the gut can cause pancreatic hypertrophy ('growth'), which is probably mediated th rough a feedback mechanism utilizing cholecystokinin. We have proposed the involvement of somatostatin, and here test the hypothesis that en dogenous somatostatin secreted into pancreatic juice may regulate panc reatic growth. Groups of rats were given the proteinase inhibitor camo state intragastrically for either 3, 7, 14, 28, or 56 days, when they were sacrificed. In some groups the pancreata were weighed and homogen ized while in other groups isolated perfused pancreatic organ preparat ions were performed. Somatostatin was measured in the homogenates, pan creatic juice and portal vein effluents. In camostate-fed animals, pan creatic weights increased to a maximum at 28 days, while pancreatic so matostatin content increased significantly from the third day onwards, and somatostatin secretion into pancreatic juice increased progressiv ely until day 28. In contrast, somatostatin secretion into portal bloo d remained unchanged from those of untreated controls over the duratio n of the experiment, and its concentration was lower than in pancreati c juice. These observations provide further evidence that endogenous p ancreatic somatostatin may control pancreatic growth in rats.