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UDP-glucuronosyltransferases 1 A (UGT1A) enzymes are capable of detoxifying a broad range of endo- and xenobiotic compounds, which contributes to antioxidative effects, modulation of inflammation and cytoprotection. In the presence of low-function genetic  UGT1A  variants fibrosis development is increased in various diseases. This study aimed to examine the role of common  UGT1A  polymorphisms in NASH. Therefore,  htgUGT1A -WT mice and  htgUGT1A -SNP mice (carrying a common human haplotype present in 10% of the white population) were fed a high-fat Paigen diet for 24 weeks. Serum aminotransferase activities, hepatic triglycerides, fibrosis development and  UGT1A  expression were assessed. Microscopic examination revealed higher hepatic fat deposition and a significant induction of  UGT1A  gene expression in  htgUGT1A -WT mice. In agreement with these observations, lower serum aminotransferase activities and lower expression levels of fibrosis-related genes were measured in  htgUGT1A -SNP mice. This was accompanied by reduced PPARα protein levels in  htgUGT1A -WT but not in SNP mice. Our data demonstrate a protective effect of a  UGT1A  SNP haplotype, leading to milder hepatic steatosis and NASH. Higher PPARα protein levels in animals with impaired UGT1A activity are the likely result of reduced glucuronidation of ligands involved in PPARα-mediated fatty acid oxidation and may lead to the observed protection in  htgUGT1A -SNP mice.

A Gilbert syndrome-associated haplotype protects against fatty liver disease in humanized transgenic mice