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  Indian J Med Microbiol
 

Figure 1: The effect of PM2.5exposure in promoting or reducing hepatic steatosis in NC- or HF-fed mice. (a) PM2.5exposure induces hepatic autophagy depending on the inflammatory pathway mediated through MyD88 and strongly represses lipid metabolism (FA oxidation and lipolysis) in the livers of mice under NC. NC diet-fed mice experienced increased hepatic steatosis since the suppression of lipolysis overweighed the anti-steatosis effect of hepatic autophagy triggered by PM2.5exposure. (b) PM2.5exposure promotes hepatic autophagy in addition to repressing lipid metabolic pathways in the livers of mice under HF diet. The anti-steatosis effect of hepatic autophagy triggered by PM2.5exposure overweighs the suppression of hepatic lipid metabolism. Thus, PM2.5-induced hepatic autophagy produces a measurable effect on alleviating hepatic steatosis in the HF-fed animals. NC: Normal chow, HF: High fat, FA: Fatty acid

Figure 1: The effect of PM<sub>2.5</sub>exposure in promoting or reducing hepatic steatosis in NC- or HF-fed mice. (a) PM<sub>2.5</sub>exposure induces hepatic autophagy depending on the inflammatory pathway mediated through MyD88 and strongly represses lipid metabolism (FA oxidation and lipolysis) in the livers of mice under NC. NC diet-fed mice experienced increased hepatic steatosis since the suppression of lipolysis overweighed the anti-steatosis effect of hepatic autophagy triggered by PM<sub>2.5</sub>exposure. (b) PM<sub>2.5</sub>exposure promotes hepatic autophagy in addition to repressing lipid metabolic pathways in the livers of mice under HF diet. The anti-steatosis effect of hepatic autophagy triggered by PM<sub>2.5</sub>exposure overweighs the suppression of hepatic lipid metabolism. Thus, PM<sub>2.5</sub>-induced hepatic autophagy produces a measurable effect on alleviating hepatic steatosis in the HF-fed animals. NC: Normal chow, HF: High fat, FA: Fatty acid