Background: Slc26a9 is a member of the Slc26 multifunctional anion transporter family with strong expression in the lung and the stomach. In the bronchial and duodenal epithelium it may function as a chloride conductance interacting with CFTR. Polymorphisms in Slc26a9 are associated with an increased incidence of meconium ileus and diabetes in cystic fibrosis patients. Aim: We investigated the expression of Slc26a9 in the pancreas and elucidated its potential role in pancreatic ductal electrolyte and fluid secretion. Methods and Results: The mRNA expression of Slc26a9 was low in pancreatic parenchyma but 20‑fold higher in microdissected pancreatic ducts. No Slc26a9 mRNA expression was detected in the liver, while bile ducts displayed low Slc26a9 expression. The main pancreatic and the common bile duct were cannulated and pancreatic and biliary fluid and bicarbonate secretion assessed in isoflurane-anesthetized Slc29 knockout mice and age- and sex‑matched wild‑type (WT) littermates in the basal state and after intravenous stimulation with secretin. Significantly reduced basal as well as secretin-stimulated pancreatic fluid secretory rates were observed in young adult (6-8 weeks) female Slc26a9 KO mice, with no difference in the bicarbonate secretory rates. In young male mice, as well as male and female old mice (>1 year), no significant difference in pancreatic ion secretion was observed, In addition, biliary fluid and bicarbonate secretion were not affected by loss of Slc26a9 expression. Conclusions: Deletion of Slc26a9 is associated with a reduction in pancreatic fluid but not bicarbonate secretion in young female mice. The results are consistent with our earlier work in the airways, stomach and duodenum which underline the importance of Slc26a9 in these epithelia particularly at young age. Once the critical age is survived, adaptation allows proper functioning of many but not all organs., For example, in cystic fibrosis patients the incidence of diabetes in higher in females.