Document Detail


Review of experimental animal models of biliary acute pancreatitis and recent advances in basic research.
MedLine Citation:
PMID:  22221567     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Acute pancreatitis (AP) is a formidable disease, which, in severe forms, causes significant mortality. Biliary AP, or gallstone obstruction-associated AP, accounts for 30-50% of all clinical cases of AP. In biliary AP, pancreatic acinar cell (PAC) death (the initiating event in the disease) is believed to occur as acinar cells make contact with bile salts when bile refluxes into the pancreatic duct. Recent advances have unveiled an important receptor responsible for the major function of bile acids on acinar cells, namely, the cell surface G-protein-coupled bile acid receptor-1 (Gpbar1), located in the apical pole of the PAC. High concentrations of bile acids induce cytosolic Ca(2+) overload and inhibit mitochondrial adenosine triphosphate (ATP) production, resulting in cell injury to both PACs and pancreatic ductal epithelial cells. Various bile salts are employed to induce experimental AP, most commonly sodium taurocholate. Recent characterization of taurolithocholic acid 3-sulphate on PACs has led researchers to focus on this bile salt because of its potency in causing acinar cell injury at relatively low, sub-detergent concentrations, which strongly implicates action via the receptor Gpbar1. Improved surgical techniques have enabled the infusion of bile salts into the pancreatic duct to induce experimental biliary AP in mice, which allows the use of these transgenic animals as powerful tools. This review summarizes recent findings using transgenic mice in experimental biliary AP.
Authors:
Mei H Wan; Wei Huang; Diane Latawiec; Kun Jiang; David M Booth; Victoria Elliott; Rajarshi Mukherjee; Qing Xia
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  HPB : the official journal of the International Hepato Pancreato Biliary Association     Volume:  14     ISSN:  1477-2574     ISO Abbreviation:  HPB (Oxford)     Publication Date:  2012 Feb 
Date Detail:
Created Date:  2012-01-06     Completed Date:  2012-05-08     Revised Date:  2013-06-26    
Medline Journal Info:
Nlm Unique ID:  100900921     Medline TA:  HPB (Oxford)     Country:  England    
Other Details:
Languages:  eng     Pagination:  73-81     Citation Subset:  IM    
Copyright Information:
© 2012 International Hepato-Pancreato-Biliary Association.
Affiliation:
Pancreatic Diseases Research Group, Department of Integrated Traditional and Western Medicine, West China Hospital, Sichuan University, Chengdu, China.
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MeSH Terms
Descriptor/Qualifier:
Acute Disease
Animals
Bile Acids and Salts / metabolism
Cholestasis / etiology*,  genetics,  metabolism,  pathology
Disease Models, Animal
Gallstones / chemically induced,  complications*,  genetics,  metabolism,  pathology
Genotype
Humans
Mice
Mice, Transgenic
Pancreatic Ducts / metabolism*,  pathology
Pancreatitis / etiology*,  genetics,  metabolism,  pathology
Phenotype
Receptors, G-Protein-Coupled / metabolism
Chemical
Reg. No./Substance:
0/Bile Acids and Salts; 0/Receptors, G-Protein-Coupled
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