Stimulation of Pancreatic Growth

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Abstract
Distal, but not proximal, resection of the small bowel induces growth of rat pancreas, but the mechanism of this phenomenon is poorly clarified. The release of cholecystokinin (CCK), a trophic hormone for the pancreas, is regulated by a negative-feedback control of bile salts. The ileum is a major site for reabsorption of bile salts. Thus, unsuppressed release of CCK due to deleted reabsorption of bile salts after distal small bowel resection may be a cause of pancreatic growth. In this study, the authors have examined whether pancreatic growth after distal small bowel resection was mediated by endogenous CCK and have determined whether the mechanism of this pancreatic growth required biosynthesis of polyamine. Male Fischer 344 rats underwent 70% distal small bowel resection or transection of the ileum. Beginning 48 hours after surgery, CR1409 (a CCK-receptor antagonist) or saline was injected subcutaneously every 8 hours. All animals were pair-fed and killed 14 days after surgery. The pancreas from each rat was excised, weighed, and assayed for DNA, RNA, protein, and polyamine content. Distal small bowel resection increased pancreatic weight, DNA, RNA, and protein, as well as polyamine levels; all of these increases were significantly suppressed by CR1409. Postprandial release of CCK into the circulation was significantly increased after distal small bowel resection. Pancreatic growth after distal small bowel resection was associated with the stimulation of polyamine biosynthesis; growth appeared to be mediated by endogenous CCK.