Endogenous CCK release and pancreatic growth in rats after feeding a proteinase inhibitor (camostate).

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Goke B, Printz H, Koop I, Rausch U, Richter G, Arnold R, Adler G

Endogenous CCK release and pancreatic growth in rats after feeding a proteinase inhibitor (camostate).

Pancreas. 1986;1(6):509-15. doi: 10.1097/00006676-198611000-00008.

PubMed ID

3562444 [ View in PubMed

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Abstract

The serine proteinase inhibitor camostate was fed to rats in single, daily doses of 100 mg/kg, 200 mg/kg, and 400 mg/kg for 5, 10, or 15 days. Within 5 days, pancreatic size and protein, DNA, and enzyme content increased significantly. After prolonged administration, this trophic effect was more pronounced, and anticoordinate regulation of the synthetic rate of individual secretory proteins was observed. While enzyme content and protein synthesis of trypsinogen and chymotrypsinogen were increased, respective values for amylase were drastically reduced. Plasma levels of cholecystokinin (CCK) did not differ from controls when measured 24 h after administration of camostate. Immediately after oral feeding of camostate, CCK levels increased 10-fold above controls, reached a maximum after 90 min, and remained elevated for more than 6 h. Proglumide, a CCK-receptor antagonist, only slightly reduced the trophic action of the proteinase inhibitor. The data indicate that endogenous CCK release by a proteinase inhibitor is as potent in the modulation of pancreatic growth and individual enzyme synthesis as exogenous hormone application.

DrugBank Data that Cites this Article

Drugs

Camostat

Drug Targets

Drug	Target	Kind	Organism	Pharmacological Action	Actions
Camostat	Cholecystokinin	Protein	Humans	Unknown	Inhibitor	Details