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Retinoic acid induced 16 deficiency exacerbates high‐fat diet‐induced steatohepatitis in mice
Author(s) -
Qian ChunLin,
Ding CuiLing,
Tang HaiLin,
Qi ZhongTian,
Wang Wen
Publication year - 2020
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.3542
Subject(s) - steatohepatitis , fatty liver , medicine , endocrinology , hepatocellular carcinoma , liver injury , cirrhosis , inflammation , retinoic acid , knockout mouse , apoptosis , biology , disease , biochemistry , receptor , gene
Non‐alcoholic fatty liver disease (NAFLD) associated with obesity may progress to non‐alcoholic steatohepatitis, cirrhosis and hepatocellular carcinoma (HCC). Retinoic acid induced 16 (RAI16) plays an important role in cell apoptosis and is also a potential marker for HCC. Here we aimed to test the effect of RAI16 deficiency on liver pathology in high‐fat diet (HFD) fed mice. Wild type (WT) and RAI16 knockout (RAI16−/−) C57BL/6 mice were fed with HFD or chow for up to 12 months. With consumption of HFD diet, RAI16−/− mice on HFD developed much more excess fatty liver within 4 months than WT mice on HFD. The expressions of fatty acid synthesis associated molecules Ppar‐γ, Srebp‐1c and Fas were further increased in RAI16−/− mice compared with WT mice on HFD. Macrophage infiltration related molecules Mcp‐1 and F4/80 and pro‐inflammatory factor Lcn2 were significantly increased in RAI16−/− mice compared with WT mice on HFD. Conclusively, RAI16 deficiency exacerbated HFD‐induced liver injury, associated with increased inflammation. These findings indicate that RAI16 plays an important role in HFD‐induced liver pathology and might be considered as a target for treatment of NAFLD. Significance 1. RAI16−/− mice on HFD developed much more excess fatty liver. 2. RAI16−/− mice showed more macrophage infiltration and proinflammation.