Ambient particulate matter (PM) newly has been regarded as a conceivable hazard for public health. A large number of studies have described that PM, exceptionally PM2.5, is correlated with respiratory, cardiovascular, and metabolic diseases, etc. PM2.5-induced hepatocyte steatosis previously has been uncovered both in cellular and murine models. Nevertheless, less is known about the underlying mechanism. Here, we found that PM2.5 could cause the downregulation of farnesoid X receptor (FXR), a key transcription factor for lipid metabolism. FXR could regulate the accumulation of lipid droplets induced by PM2.5 in vitro. Moreover, FXR-/- mice were exposed to PM2.5 for 2 months to investigate the role of FXR in pathogenesis of PM2.5-induced hepatic steatosis in vivo. The results showed that exposure of wild-type (WT) mice to PM2.5 caused mild liver steatosis compared with the mice exposure to filtered air (FA). Furthermore, the content of triglyceride (TG) and total cholesterol (TC) was elevated in WT mice liver triggered by the inhalation of PM2.5. However, there was no statistical difference in TG and TC content between FXR-/- mice with and without PM2.5 exposure. Overall, our finding suggested FXR mediated PM2.5-induced hepatic steatosis.
Keywords: Air pollution; Farnesoid X receptor; Fatty liver; Hepatic steatosis; Nuclear receptor; PM2.5.