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- W3168889752 abstract "Obesity-associated nonalcoholic fatty liver disease (NAFLD) is characterized by a continuum of pathological changes in the liver. Although progression from simple steatosis to the inflammatory stage of NAFLD (i.e. nonalcoholic steatohepatitis/NASH) represents a critical switch from a benign to a harmful status in the progression of NAFLD, the mechanism underlying this switch is little understood. As sphingosine kinase 1 (SK1) catalyzes the biosynthesis of sphingosine-1-phosphate, a lipid implicated in inflammation, we hypothesized that deficiency of SK1 might prevent the progression from simple steatosis to NASH in diet-induced obesity. We thus administrated SK1-deficient and wild type mice with both high fat diet (HFD) and isocaloric low fat control diet. Results SK1 deficiency diminished HFD-induced pathological changes, including severe lipid accumulation and macrosteatosis, increases in serum alanine aminotransferase activity, immune cell infiltration into liver parenchyma, and induction of inflammatory cytokines. Moreover, SK1 deficiency also attenuated HFD induction of prosteatotic and proinflammatory genes in the liver. Conclusion SK1 is essential to progression from simple steatosis into NASH in diet-induced obesity. Funding: a VA Merit award and the NIH COBRE in Lipidomics and Pathobiology (P20RR017677), both to LAC, and NIH Grant 1R01DK069369 to KDC." @default.
- W3168889752 created "2021-06-22" @default.
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- W3168889752 date "2013-04-01" @default.
- W3168889752 modified "2023-09-27" @default.
- W3168889752 title "Deficiency of sphingosine kinase 1 ameliorates hepatic steatosis and inflammation in diet‐induced obesity" @default.
- W3168889752 doi "https://doi.org/10.1096/fasebj.27.1_supplement.1010.15" @default.
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