@article{TEXTUAL,
      recid = {6625},
      author = {Cho, Sungjoon and Tripathi, Ashutosh and Chlipala, George  and Green, Stefan and Lee, Hyunwoo and Chang, Eugene B. and  Jeong, Hyunyoung},
      title = {Fructose diet alleviates acetaminophen-induced  hepatotoxicity in mice},
      journal = {PLOS ONE},
      address = {2017-08-23},
      number = {TEXTUAL},
      abstract = {Acetaminophen (APAP) is a commonly used analgesic and  antipyretic that can cause hepatotoxicity due to production  of toxic metabolites via cytochrome P450 (Cyp) 1a2 and  Cyp2e1. Previous studies have shown conflicting effects of  fructose (the major component in Western diet) on the  susceptibility to APAP-induced hepatotoxicity. To evaluate  the role of fructose-supplemented diet in modulating the  extent of APAP-induced liver injury, male C57BL/6J mice  were given 30% (w/v) fructose in water (or regular water)  for 8 weeks, followed by oral administration of APAP.  APAP-induced liver injury (determined by serum levels of  liver enzymes) was decreased by two-fold in mice pretreated  with fructose. Fructose-treated mice exhibited (~1.5 fold)  higher basal glutathione levels and (~2 fold) lower basal  (mRNA and activity) levels of Cyp1a2 and Cyp2e1, suggesting  decreased bioactivation of APAP and increased  detoxification of toxic metabolite in fructose-fed mice.  Hepatic mRNA expression of heat shock protein 70 was also  found increased in fructose-fed mice. Analysis of bacterial  16S rRNA gene amplicons from the cecal samples of vehicle  groups showed that the fructose diet altered gut bacterial  community, leading to increased α-diversity. The abundance  of several bacterial taxa including the genus Anaerostipes  was found to be significantly correlated with the levels of  hepatic Cyp2e1, Cyp1a2 mRNA, and glutathione. Together,  these results suggest that the fructose-supplemented diet  decreases APAP-induced liver injury in mice, in part by  reducing metabolic activation of APAP and inducing  detoxification of toxic metabolites, potentially through  altered composition of gut microbiota.},
      url = {http://knowledge.uchicago.edu/record/6625},
}