STIMULATION OF PANCREATIC GROWTH - DISTAL SMALL-BOWEL RESECTION MEDIATED BY INCREASED LEVELS OF CHOLECYSTOKININ

Summ. Background Data Distal, but not proximal, resection of the small bower induces growth of rat pancreas, but the mechanism of this pheno menon is poorly clarified. The release of cholecystokinin (CCK), atrop hic hormone for the pancreas, is regulated by a negative-feedback cont rol of bile salts. The ileum is a major site for reabsorption of bile salts. Thus, unsuppressed release of CCK due to deleted reabsorption o f bile salts after distal small bowel resection may be a cause of panc reatic growth. In this study, the authors have examined whether pancre atic growth after distal small bowel resection was mediated by endogen ous CCK and have determined whether the mechanism of this pancreatic g rowth required biosynthesis of polyamine. Methods Male Fischer 344 rat s underwent 70% distal small bowel resection or transection of the ile um. Beginning 48 hours after surgery, CR1409 (a CCK-receptor antagonis t) or saline was injected subcutaneously every 8 hours. All animals we re pair-fed and kited 14 days after Surgery. The pancreas from each ra t was excised, weighed, and assayed for DNA, RNA, protein, and polyami ne content. Results Distal small bower resection increased pancreatic weight, DNA, RNA, and protein, as well as polyamine levels; all of the se increases were significantly suppressed by CR1409. Postprandial rel ease of CCK into the circulation was significantly increased after dis tal small bowel resection. Conclusions Pancreatic growth after distal small bowel resection was associated with the stimulation of polyamine biosynthesis; growth appeared to be mediated by endogenous CCK.