Bile acids and pancreatic disease

Morihisa Hirota, Tooru Shimosegawa

Research output: Chapter in Book/Report/Conference proceedingChapter

2 Citations (Scopus)


It is generally believed that biliary acute pancreatitis is initiated by contact between bile acid and pancreatic acinar cells due to bile reflux into the pancreatic duct followed by the impaction of a gallstone into the papilla of Vater, although it is still debatable. Several animal models of biliary acute pancreatitis have been established and used to elucidate the molecular mechanisms by which bile acids induce acute pancreatitis. The bile acids enter the acinar cells through transporters on the plasma membrane and induce sustained Ca2+ influx into the cytosol from acidic stores in the apical portion and from the endoplasmic reticulum in the basal portion of the cells. The intercellular Ca2+ overload leads to acinar cell necrosis subsequent to mitochondrial depolarization. A receptor Gbpa1-mediated bile acid signaling has also been demonstrated to play an important role in the bile acid-induced acinar cell injury. Pancreatic fluid secretion from ductal cells is influenced by the bile acids in a concentration-dependent manner, with a stimulatory effect at low concentrations and an inhibitory effect at high concentrations. It is expected to develop a specific medicine to prevent bile acids-induced acute pancreatitis.

Original languageEnglish
Title of host publicationBile Acids in Gastroenterology
Subtitle of host publicationBasic and Clinical
PublisherSpringer Japan
Number of pages8
ISBN (Electronic)9784431560623
ISBN (Print)9784431560609
Publication statusPublished - 2017 Apr 3


  • Acute pancreatitis
  • Bile acid
  • Biliary acute pancreatitis
  • Calcium
  • Necrosis

ASJC Scopus subject areas

  • Medicine(all)


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