Retinoic acid induced 16 deficiency exacerbates high-fat diet-induced steatohepatitis in mice.

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.

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