Insulin potentiates cholecystokinin (CCK)-induced secretion of pancreatic kallikrein.
The effects of insulin on pancreatic kallikrein secretion were studied in streptozotocin diabetic rats and after acute administration of insulin to normal rats. Studies on total protein and amylase secretion were included for comparison. In diabetic rats, the concentration of amylase in pancreatic tissue as well as basal and CCK-stimulated amylase exocrine secretion were significantly reduced. Insulin treatment restored pancreatic tissue concentration and exocrine release of amylase to normal. Insulin deficiency did not induce any change in the concentration of kallikrein or trypsin-like activity in pancreatic tissue. However, basal kallikrein secretion was higher in diabetic rats than in controls. Insulin treatment of diabetics rats did not alter basal kallikrein secretion but potentiated CCK-stimulation of kallikrein release. In normal rats, CCK induced an increase of pancreatic protein, amylase, and kallikrein secretion but not pancreatic juice flow. Additional administration of insulin potentiated the CCK-induced secretory rate of pancreatic juice, protein, and kallikrein but not amylase. A 1.6 times higher concentration of kallikrein was found in the portal vein than in arterial blood, indicating an endocrine release of pancreatic kallikrein. No difference in the concentration of circulating kallikrein was observed between the control and the insulin-treated group.
Berg
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T
Johansen
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Brekke
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D000681:Amylases / Q000378:metabolism; D000818:Animals; D002766:Cholecystokinin / Q000494:pharmacology*; D003921:Diabetes Mellitus, Experimental / Q000201:enzymology; D004357:Drug Synergism; D007328:Insulin / Q000494:pharmacology*; D007610:Kallikreins / Q000378:metabolism*; D008297:Male; D010179:Pancreas / Q000187:drug effects / Q000201:enzymology*; D051381:Rats; D011921:Rats, Inbred WKY; D014357:Trypsin / Q000378:metabolism
D007328:Insulin; D002766:Cholecystokinin; D000681:Amylases; D007610:Kallikreins; D014357:Trypsin