Abstract

The aim of this study was to elucidate the mechanism of chronic biliary diversion and its effect on pancreatic growth. In the first part of the study, nine mongrel dogs underwent diversion of bile from the gastrointestinal tract by ligating the common bile duct and interposing a segment of jejunum between the gallbladder and the urinary bladder (cholecystojejunocystostomy [CJC]). Despite the loss of 7% of their body weight at 12 weeks after bilioenteric diversion, CJC dogs had significantly greater pancreatic wet weight than control dogs (51.2 ± 2.2 g vs. 37.1 ± 2.2 g). In the second part of the study, six other dogs underwent CJC. Twelve weeks later, bilioenteric continuity was restored by creating a cholecystojejunoduodenostomy (CJD). The dogs were given butter (3 g/kg) by mouth (prior to surgery, 12 weeks after CJC, and 4 weeks after CJD). Pancreatic excisional biopsy specimens were obtained at each operation and at autopsy. CJC induced more pancreatic RNA per milligram of weight (743 ± 52, CJC; 579 ± 44, prior to surgery, P <0.05 vs. CJC; 520 ± 26 μg/100 mg · tissue, CJD, P <0.01 vs. CJC), but not more DNA, and significantly higher basal plasma cholecystokinin levels and butter-stimulated cholecystokinin responses when compared with values prior to surgery or following CJD. We conclude that chronic biliary diversion induces pancreatic growth associated with hypersecretion of cholecystokinin in dogs.

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