Airborne fine particulate matter in Japan induces lipid synthesis and inhibits autophagy in HepG2 cells.

Inhalation of particulate matter with a diameter less than 2.5 µm has been reported to exacerbates fatty liver disease. However, the components and mechanisms of particulate matter involved in hepatic lipid metabolism and autophagy have not been fully elucidated. We found that atmospheric particulate matter in Japan stimulated lipogenesis in hepatocytes even when its lipid component was removed. Furthermore, we demonstrated that particulate matter did not promote autophagosome formation but inhibited autophagic degradation in hepatocytes. In previous toxicity experiments, particulate matter collected from atmosphere often contained contaminants originating from filters. In this study, we exposed the powdery particulate matter with less contaminants collected using a cyclone and impactor system to HepG2 cells, human hepatocyte. This particulate matter induced lipogenesis and endoplasmic reticulum stress in HepG2 cells as well as previous reports of particulate matter in the USA and China. On the other hand, when autophagic flux were examined in detail, the particulate matter did not promote autophagosome formation, but inhibited autophagic degradation. Since these effects were similar to those of palmitate, a fatty acid, we prepared particulate matter in which lipid component was removed by acetone and compared the effects on HepG2 cells with those of untreated one. The particulate matter without lipid component induced lipid droplets as well as did the untreated one although it induced less endoplasmic reticulum stress. These results suggest that hepatic lipid synthesis is stimulated not only by the uptake of lipid but also by other components in the particulate matter.