Increased CCK-Response to Proteinase Inhibitor Feeding After Induction of Pancreatic Hypertrophy in Rats

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Abstract
Repeated intragastric instillation of a trypsin inhibitor (camostate) to rats resulted in pancreatic growth. This was ascribed to the trophic effect of endogenously released cholecystokinin (CCK). We evaluated the CCKreleasing potency of different doses of camostate (50400 mg/kg body weight administered perorally) during the course of experimentally induced pancreatic growth. Significant increments of pancreatic weight and protein and trypsin content of the pancreata were observed after 5 days of camostate treatment; changes were further pronounced after 10 days. Juice flow and protein and trypsin output from the hypertrophied pancreata were enhanced after 5 days. These effects were diminished after 10 days of camostate treatment. The direct increase in plasma CCK in response to camostate after pretreatments by daily oral doses of 200 mgkg camostate over 5 or 10 days was more pronounced in rats with pancreatic hypertrophy compared with untreated controls. These findings mirror possible adaptation of CCK-releasing cells to “desensitisation” of acinar cells after pancreatic hypertrophy.