Figure 5.

The working models for the effect of PM_2.5 exposure in promoting or relieving hepatic steatosis in mice under NC or HFD. (A) The effects and pathways by which inhalation exposure to PM_2.5 represses lipid metabolic and anti-inflammatory pathways, and induces hepatic autophagy in the livers of mice under NC. Because the repression of hepatic lipid metabolic pathways overweigh the anti-steatosis effect of hepatic autophagy triggered by PM_2.5 exposure, the NC-fed mice exhibited increased hepatic steatosis upon PM_2.5 exposure. (B) The effects and pathways by which PM_2.5 exposure and HF feeding repress or promote hepatic autophagy, lipid metabolic and anti-inflammatory pathways in the livers of mice under HFD. Because HF feeding represses hepatic autophagy or lipophagy, a major cause of HF-induced hepatic steatosis, PM_2.5-triggered hepatic autophagy exerts a discernable effect on mitigating hepatic steatosis in the HF-fed animals. The illustrations were generated by using Adobe Illustrator software.