Farnesoid X receptor mediates hepatic steatosis induced by PM2.5

• Published in: Environmental science and pollution research international Vol. 27; no. 27; pp. 34412 - 34420
• Main Authors: Wang, Mengyao, Tan, Jieqiong, Zhou, Ji, Yi, Bin, Huang, Zhijun
• Format: Journal Article
• Language: English
• Published: Berlin/Heidelberg Springer Berlin Heidelberg 01-09-2020; Springer Nature B.V
• Subjects: Adipocytes; Adipogenesis; Adipose tissue; Aquatic Pollution; Aromatic compounds; Atmospheric Protection/Air Quality Control/Air Pollution; Beta cells; Cytochrome P450; Diabetes; Diabetes mellitus; Dioxins; Earth and Environmental Science; Ecotoxicology; Environment; Environmental Chemistry; Environmental factors; Environmental Health; Environmental science; Human behavior; Hydrocarbons; Hypertrophy; Inflammation; Inflammatory response; Inhalation; Metabolic disorders; NF-κB protein; Particulate matter; PCB; Pollutants; Polychlorinated biphenyls; Preadipocytes; Public health; Research Article; Waste Water Technology; Water Management; Water Pollution Control; Farnesoid X receptor; Air pollution; Nuclear receptor; Fatty liver; Hepatic steatosis; PM
• ISSN: 0944-1344; 1614-7499
• DOI: 10.1007/s11356-020-09676-2

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 PM
2.5
, is correlated with respiratory, cardiovascular, and metabolic diseases, etc. PM
2.5
-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 PM
2.5
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 PM
2.5
in vitro. Moreover, FXR
−/−
mice were exposed to PM
2.5
for 2 months to investigate the role of FXR in pathogenesis of PM
2.5
-induced hepatic steatosis in vivo. The results showed that exposure of wild-type (WT) mice to PM
2.5
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 PM
2.5
. However, there was no statistical difference in TG and TC content between FXR
−/−
mice with and without PM
2.5
exposure. Overall, our finding suggested FXR mediated PM
2.5
-induced hepatic steatosis.