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A major alteration found in the present work is the substantial increase in glucuronides in the blood of cirrhotic mice, which is explained by high levels of the sinusoidal export carriers Abcc3 and Abcc4 that are known to be upregulated in cholestatic liver disease and act by exporting bile acids from hepatocytes to avoid an increase beyond cytotoxic levels ( 4 administered for 1 year underwent severe cholestasis with increased Abcc3 and Abcc4 levels, which corresponds to the findings of previous studies ( A surprising result was the robustness of phase I metabolism in cirrhotic mice, exemplified by the metabolism of caffeine to paraxanthine by the phase I enzyme Cyp1a2 in healthy mice