Modulation of transport and metabolism of bile acids and bilirubin by chlorogenic acid against hepatotoxicity and cholestasis in bile duct ligation rats: involvement of SIRT1‐mediated deacetylation of FXR and PGC‐1α

Modulation of transport and metabolism of bile acids and bilirubin by chlorogenic acid against... IntroductionObstructive jaundice results from increased serum bilirubin levels due to obstruction of bile flow from blockage of the large bile ducts. Obstructive jaundice is commonly due to benign common choledocholithiasis, biliary stricture, cholangitis, pancreaticobiliary malignancies, and metastatic disease . Patients with obstructive jaundice have various pathophysiological changes that affect various organs and physiologic processes. Due to dysfunctional bile excretion, the accumulation of high levels of bilirubin and bile acids (BAs) in the hepatocytes causes acute liver injury as the initial response to oxidative stress , followed by disorder of multiple systems including kidney failure, cardiac dysfunction, hemostatic abnormalities, and altered immunity .Although the exact mechanisms involved in the multiple organ dysfunction caused by obstructive jaundice still remains unclear, the disruption of bilirubin and BAs homeostasis may be, at least in part, an important cause . Bilirubin and BAs homeostasis is maintained by the hepatobiliary transport and metabolism system in the liver . At first, free bilirubin, cholesterol, and BAs are uptaken into hepatocytes via passive diffusion or transporter‐mediated transmembrane transport systems, which include several uptake transporters from the solute carrier (SLC) superfamily (such as the Na+‐taurocholate cotransporting polypeptide [NTCP]) . Then, bilirubin, cholesterol, and BAs are exposed to phase http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Journal of Hepato-Biliary-Pancreatic Sciences Wiley

Modulation of transport and metabolism of bile acids and bilirubin by chlorogenic acid against hepatotoxicity and cholestasis in bile duct ligation rats: involvement of SIRT1‐mediated deacetylation of FXR and PGC‐1α

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Publisher
Wiley Subscription Services, Inc., A Wiley Company
Copyright
Copyright © 2018 Japanese Society of Hepato‐Biliary‐Pancreatic Surgery
ISSN
1868-6974
eISSN
1868-6982
D.O.I.
10.1002/jhbp.537
Publisher site
See Article on Publisher Site

Abstract

IntroductionObstructive jaundice results from increased serum bilirubin levels due to obstruction of bile flow from blockage of the large bile ducts. Obstructive jaundice is commonly due to benign common choledocholithiasis, biliary stricture, cholangitis, pancreaticobiliary malignancies, and metastatic disease . Patients with obstructive jaundice have various pathophysiological changes that affect various organs and physiologic processes. Due to dysfunctional bile excretion, the accumulation of high levels of bilirubin and bile acids (BAs) in the hepatocytes causes acute liver injury as the initial response to oxidative stress , followed by disorder of multiple systems including kidney failure, cardiac dysfunction, hemostatic abnormalities, and altered immunity .Although the exact mechanisms involved in the multiple organ dysfunction caused by obstructive jaundice still remains unclear, the disruption of bilirubin and BAs homeostasis may be, at least in part, an important cause . Bilirubin and BAs homeostasis is maintained by the hepatobiliary transport and metabolism system in the liver . At first, free bilirubin, cholesterol, and BAs are uptaken into hepatocytes via passive diffusion or transporter‐mediated transmembrane transport systems, which include several uptake transporters from the solute carrier (SLC) superfamily (such as the Na+‐taurocholate cotransporting polypeptide [NTCP]) . Then, bilirubin, cholesterol, and BAs are exposed to phase

Journal

Journal of Hepato-Biliary-Pancreatic SciencesWiley

Published: Jan 1, 2018

Keywords: ; ; ; ; ;

References

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