Ambient fine particulate matter disrupts hepatic circadian oscillation and lipid metabolism in a mouse model

Emerging evidence has shown that exposure to ambient fine particulate matter (PM_2.5) is associated with hepatic lipid accumulation. However, the underlying mechanism is not fully characterized yet. Autonomous circadian clock in the liver plays a fundamental role in maintaining lipid metabolism homeostasis. In this study, we evaluated the effects of ambient PM_2.5 exposure on the expression of hepatic circadian clock genes and expression rhythm of genes associated with lipid metabolism in mice liver. Male C57BL/6 mice were randomly assigned to ambient PM_2.5 or filtered air for 10 weeks via a whole body exposure system. We found that the liver mass was reduced significantly at zeitgeber time (ZT) 8 in mice exposed to PM_2.5 but not levels or circadian rhythm of hepatic triglycerides or free fatty acid (FFA). In addition, exposure to PM_2.5 led to enhanced expression of bmal1 at ZT0/24, cry1 at ZT16 and rev-erbα at ZT4 and ZT8. Furthermore, the expression of pparα was enhanced in mice liver at ZT4 and ZT8 after PM_2.5 exposure, with upregulation of pparα-mediated genes responsible for fatty acid transport and oxidation. Finally, the expression of rate-limiting enzymes for lipid synthesis was all significantly increased in the liver of PM_2.5 exposed mice at ZT12. Therefore, the present study provides new perspectives for revealing the etiology of hepatic lipid metabolism abnormality from PM_2.5-induced circadian rhythm disorder.

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