Diversion of pancreatic-biliary (PB) secretions in rats for 23 days led to loss of enterokinase (EK) activity in bypassed segments of the small intestine. Simultaneous oral trypsinogen and bile salt (TB) supplements prevented the loss of EK activity. To study the temporal course of events after PB diversion and to determine if the loss of EK is reversible, PB diversion was performed in rats by surgical transposition of the 4-cm segment of duodenum including the ampulla of Vater to a point 30 cm distal to its original site. Bypassed and control (sham- and nonoperated) rats fed standard rat chow were sacrificed at 10, 23, and 45 days after surgery. One bypassed group was fed standard chow for 23 days and then chow supplemented with TB until sacrifice at 45 days. At sacrifice, the intestines were divided into segment 1 (the bypassed proximal 30 cm) and segment 2 (the 30 cm distal to the bypass). In segment 1, EK disappeared almost completely by 10 days and remained at the same low levels at both 23 and 45 days (p less than 0.05). No significant changes in EK levels were found at any time in segment 2 distal to the bypass. Mucosal disaccharidase activity in segment 1 increased or showed no change. In rats with delayed TB supplementation, EK activity in segment 1 returned almost to control levels at the time of sacrifice. The results confirm the importance of PB secretions in the maintenance of EK activity. The effects of bypass on EK are both enzyme- and site-specific.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic diversion of pancreatic and biliary secretions away from the proximal small intestine resulted in rapid increases in pancreatic size and protein content in adult rats. The effect was detectable as early as 10 days postsurgery. Differential changes in pancreatic enzymes were evident after bypass. The concentration of trypsinogen remained stable while amylase concentrations showed a marked decrease. Total pancreatic trypsinogen content, however, was increased, while amylase content remained similar to controls. Feeding bypassed rats with chows containing various pancreatic and biliary supplements had no effect on the hyperplastic response of their pancreata. Trypsinogen and amylase levels in supplemented groups remained similar to the bypassed group fed nonsupplemented chow, with the exception of increases in trypsinogen concentration and content in the groups supplemented with bile and cotazyme plus bile acids. The adequacy of oral refeeding of pancreatic biliary components was supported by its effectiveness in restoring mucosal enterokinase activity and trypsin levels in segment 1. However, there was no correlation between tryptic activity in the contents of the bypassed segment and the eventual pancreatic weight. These results indicate that factors other than those supplemented in this study are required in maintaining the steady state of pancreatic growth in normal rats.