Emerging evidence supports that exposure to ambient fine particulate matter (PM2.5) is associated with the metabolic syndrome. As the main neuroendocrine axis in mammals, the hypothalamic-pituitary-adrenal (HPA) axis's circadian rhythm (CR) plays an essential role in regulating metabolic homeostasis. Our previous studies found that ambient PM2.5 exposure caused CR disorder of the critical enzymes involved in lipid metabolism in mouse liver and adipose tissues. However, the impact of ambient PM2.5 exposure on the HPA axis is not fully illustrated yet. Male C57BL/6 mice were randomly exposed to ambient PM2.5 or filtered air for ten weeks via a whole-body exposure system. Rhythmic oscillations of clock genes in the hypothalamus and adrenal gland were characterized. The effects of ambient PM2.5 exposure on clock gene expression and rhythmic expression of molecules related to glucocorticoid synthesis were also examined. Firstly, a more robust CR of clock genes was demonstrated in the adrenal gland than that in the hypothalamus. Secondly, PM2.5 exposure significantly inhibited the expression of Clock at ZT8 in the hypothalamus. However, both circadian oscillation and expression levels of Bmal1, Cry1, Cry2, and Rorα were increased significantly by ambient PM2.5 exposure in the adrenal gland. Moreover, abnormal rhythmic oscillation patterns of corticotropin-releasing hormone and adrenocorticotropic hormone were observed after ambient PM2.5 exposure, with no change at the expression levels. Finally, the expression of Cyp11b1 was markedly decreased at ZT0 in the adrenal gland of PM2.5 exposed mice. Our findings provide new insights into the ambient PM2.5 exposure-induced metabolic syndrome from the perspective of CR disturbances.
Keywords: Adrenal gland; Circadian rhythm; Fine particulate matter; Hypothalamus.
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