Jan 1, 1988

Increased CCK-response to proteinase inhibitor feeding after induction of pancreatic hypertrophy in rats

B GökeG Adler


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 CCK-releasing potency of different doses of camostate (50-400 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 mg/kg 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.

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Mentioned in this Paper

Trypsin Inhibitors
August Rats
Cholecystokinin Measurement
Weighing Patient
Proteinase inhibitor (substance)

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