Air pollution was becoming a global threat to the public health, which was primarily mediated by PM2.5 induced cardiovascular diseases and pulmonary diseases. Recently, observational epidemiologic studies proposed the link between PM2.5 and obesity. Consistently, the link was also supported by limited animal researches. However, the potential mechanism mediating the harmful effects of PM2.5 was still elusive. In this study, we applied the "real-ambient exposure" system to conduct the experiments, which was closer to the status of ambient air pollution compared with the method of intratracheal instillation and concentrated air particles (CAPs) exposure system. Nuclear factor E2-related factor 2 (Nrf2) was previously reported to protect against inflammation and oxidative stress when exposed to PM2.5. Here, we reported that Nrf2-/- mice developed overgrowth of adipose tissue after "real-ambient exposure" to PM2.5, compared to filtered air (FA) group. Consistently, compared to FA group, adipocytes from subcutaneous (sWAT) and gonadal (gWAT) white adipose tissue of Nrf2-/- mice exhibited enlarged cell size in PM2.5 exposure group. Furthermore, the levels of high-density lipoprotein (HDL) and low-density lipoprotein (LDL) in serum and liver of Nrf2-/- mice were also altered statistically in PM2.5 exposure group. Importantly, when the expression of lipogenic enzymes was analyzed, the levels of the related specific genes in adipose tissue and liver of Nrf2-/- mice were altered in PM2.5 exposure group. Interestingly, the key transcription factors modulating expression of lipogenic enzymes in liver of Nrf2-/- mice were also found altered in PM2.5 exposure group, such as peroxisome proliferator-activated receptor (PPARα, PPARγ). Taken together, our study mimicked the status of ambient air pollution, revealed new insights into the adverse effect of PM2.5 exposure, provided new link between air pollution and overgrowth of adipose tissue, and supported the vital role of Nrf2 in mediating the side effects of PM2.5.
Keywords: Adipose tissue; Lipid homeostasis; Nrf2; PM(2.5).
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