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It remains unclear how hepatic steatosis links to inflammation. Leukocyte cell-derived chemotaxin 2 (LECT2) is a hepatokine that senses fat in the liver and is upregulated prior to weight gain. The aim of this study was to investigate the significance of LECT2 in the development of nonalcoholic steatohepatitis (NASH). In human liver biopsy samples, elevated  LECT2  mRNA levels were positively correlated with body mass index (BMI) and increased in patients who have steatosis and inflammation in the liver.  LECT2  mRNA levels were also positively correlated with the mRNA levels of the inflammatory genes  CCR2  and  TLR4 . In C57BL/6J mice fed with a high-fat diet, mRNA levels of the inflammatory cytokines  Tnfa  and  Nos2  were significantly lower in  Lect2  KO mice. In flow cytometry analyses, the number of M1-like macrophages and M1/M2 ratio were significantly lower in  Lect2  KO mice than in WT mice. In KUP5, mouse kupffer cell line ,  LECT2 selectively enhanced the LPS-induced phosphorylation of JNK, but not that of ERK and p38. Consistently, LECT2 enhanced the LPS-induced phosphorylation of MKK4 and TAB2, upstream activators of JNK. Hepatic expression of LECT2 is upregulated in association with the inflammatory signature in human liver tissues. The elevation of LECT2 shifts liver residual macrophage to the M1-like phenotype, and contributes to the development of liver inflammation. These findings shed light on the hepatokine LECT2 as a potential therapeutic target that can dissociate liver steatosis from inflammation.

LECT2 as a hepatokine links liver steatosis to inflammation via activating tissue macrophages in NASH