AI Article Synopsis
- Obstructive cholestasis leads to liver damage by causing toxic bile acids to build up, which current animal models struggle to accurately represent.
- Research on Gold Syrian hamsters showed that their biochemical responses to bile duct ligation matched those seen in human cholestatic patients, including changes in bile acid management and slower progression to liver fibrosis.
- The study found that hamsters adapt to cholestasis without severe liver cell death, preserving energy levels and exhibiting a protective response similar to that in humans, suggesting that they are valuable models for studying cholestatic liver disease.
Article Abstract
Obstructive cholestasis causes liver injury via accumulation of toxic bile acids (BAs). Therapeutic options for cholestatic liver disease are limited, partially because the available murine disease models lack translational value. Profiling of time-related changes following bile duct ligation (BDL) in Gold Syrian hamsters revealed a biochemical response similar to cholestatic patients in terms of BA pool composition, alterations in hepatocyte BA transport and signaling, suppression of BA production, and adapted BA metabolism. Hamsters tolerated cholestasis well for up to 28days and progressed relatively slowly to fibrotic liver injury. Hepatocellular necrosis was absent, which coincided with preserved intrahepatic energy levels and only mild oxidative stress. The histological response to cholestasis in hamsters was similar to the changes seen in 17 patients with prolonged obstructive cholestasis caused by cholangiocarcinoma. Hamsters moreover upregulated hepatic fibroblast growth factor 15 (Fgf15) expression in response to BDL, which is a cytoprotective adaptation to cholestasis that hitherto had only been documented in cholestatic human livers. Hamster models should therefore be added to the repertoire of animal models used to study the pathophysiology of cholestatic liver disease.
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| http://dx.doi.org/10.1016/j.bbadis.2017.11.022 | DOI Listing |
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