Figure 1.

The proposed role of RELMβ in the pathogenesis of NAFLD/NASH. Intake of a high-fat diet and obesity increase both intestinal expression and circulating levels of resistin like molecule β (RELMβ). Circulating RELMβ elicits insulin resistance, and increased gut-derived RELMβ and gut microbiota appear to regulate each other, thereby increasing translocation of the endotoxin lipopolysaccharide (LPS) from the intestine into the bloodstream and liver, which induces hepatic steatosis and inflammation. In the liver, RELMβ in Kupffer cells exacerbates hepatic inflammation, along with endotoxemia, which further worsens non-alcoholic fatty liver disease (NAFLD)/non-alcoholic steatohepatitis (NASH).