Exocrine pancreatic function in oleic acid-induced pancreatic insufficiency in rats.
Pancreatic insufficiency was induced in rats by a single injection of 50 microliter oleic acid into the pancreatic duct over a period of 3 min. Exocrine tissue was destroyed within 3-6 days, and after 6 weeks the remaining pancreas equaled 2.7% of the original organ. The rats showed retardation of body weight in spite of normal food intake. After 7 weeks the fecal weight increased by 23%, and the fecal chymotrypsin activity decreased by 90% compared to controls. At this time plasma cholecystokinin (CCK) concentrations were significantly elevated. The amylase content in the remaining pancreas was reduced by 99%, and trypsin content was reduced by 93%. Unstimulated protein discharge from the remnant pancreas in vitro was threefold higher compared to secretion from control tissue. Thus a simple, reproducible model for inducing persistent pancreatic insufficiency was developed. To compensate for the loss of exocrine tissue, the remaining acinar cells adapt by a CCK-mediated increase in protein secretion.
D000222:Adaptation, Physiological; D000681:Amylases / Q000378:metabolism; D000818:Animals; D002766:Cholecystokinin / Q000097:blood; D004064:Digestive System / Q000503:physiopathology; D004195:Disease Models, Animal; D008297:Male; D019301:Oleic Acid; D009829:Oleic Acids; D010182:Pancreatic Diseases / Q000139:chemically induced* / Q000473:pathology / Q000503:physiopathology; D051381:Rats; D011919:Rats, Inbred Strains; D014362:Trypsinogen / Q000378:metabolism
D009829:Oleic Acids; D019301:Oleic Acid; D014362:Trypsinogen; D002766:Cholecystokinin; D000681:Amylases