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Retrograde intraductal infusion of TLCS (50 ¦Ìl, 3 mM) and repeated administration ofcaerulein (50 ¦Ìg/injection, 12 injections) each induce acute pancreatitis that is characterized by hyperamylasemia, pancreatic edema, inflammation, and acinar cell injury/necrosis (Fig. 2Aand B). In TLCS-induced pancreatitis, hyperamylasemia, pancreatic edema, pancreaticinflammation and acinar cell injury/death are all significantly reduced (p<0.05) whenGpbar1 has been deleted (Fig. 2A) but, when pancreatitis is induced by caeruleinadministration, none of these parameters of pancreatitis severity are altered by genetic deletionof Gpbar1 (Fig. 1B). None of the features of TLCS-induced pancreatitis (i.e. hyperamylasemia,edema, and acinar cell injury/death) are observed when 50 ¦Ìl of 3 mM Na-taurocholate, ratherthan TLCS, is infused into the pancreatic duct (Suppl. Fig. 2A).

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