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Abstract: ObjectiveTo explore the mechanism of Fam172a gene knockout in enhancing endoplasmic reticulum stress (ERS) induced nonalcoholic fatty liver disease (NAFLD). Methods Mice were intraperitoneally injected with PBS, tunicamycin ( TM), or the NF-κB inhibitor DHMEQ. The hepatic function and hepatic lipid accumulation were then evaluated, and protein levelswere assessed via Western blotting. Results Compared to the control group, the Fam172a ^{- / -} -TMgroup had significantly increased levels of serum ALT and AST, along with the increased liver structure damage and lipid accumulation. Additionally, the relative expression levels of GRP78, CHOP,and pNF-κB / NF-κB in liver tissues were significantly up-regulated in the Fam172a ^{- / -} -TM group. Furthermore, DHMEQ significantly reduced liver injury, lipid accumulation, and ERS inFam172a ^{- / -} mice. Conclusion Fam172a knockout could enhance the ERS-induced NAFLD byactivation of NF-κB pathway.

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