Asprosin aggravates nonalcoholic fatty liver disease via inflammation and lipid metabolic disturbance mediated by ROS

Abstract

Abstract Asprosin (ASP) is a newly-identified adipokine and plays important roles in energy metabolism homeostasis. However, there is no report on whether and how ASP is involved in the pathogenesis of nonalcoholic fatty liver disease (NAFLD). Therefore, in this study, we investigated the role and the underlying mechanisms of ASP in the cell and mouse models of NAFLD. Our data showed that ASP-deficiency significantly alleviated HFD-induced inflammation and NAFLD, inhibited the hepatic fat deposition and down-regulated the expressions of fat acid synthase (FASN), peroxisome proliferator-activated receptor γ (PPARγ) and forkhead box protein O1 (FOXO1) in the ASP-deficiency mouse model, suggesting that ASP is involved in the pathogenesis of NAFLD. Moreover, we found that the mechanism of ASP responsible for NAFLD was through disturbing the lipid metabolism homeostasis of hepatocytes and promoting the inflammation mediated by ROS. The findings suggest that ASP would become a diagnostic marker and therapeutic target for NAFLD.