PPARα suppresses low-intensity-noise-induced body weight gain in mice: the aggravation of fatty liver is covered up

Abstract

Abstract Background As the second risky environmental pollution, noise imposes threats to human health. Exposure to high-intensity noise causes hearing impairment, psychotic disorders, endocrine modifications. However, the relationship among low-intensity noise, obesity and lipid-regulating nuclear factor PPARα is not yet clear.Methods In this study, wild-type (WT) and Pparα-null (KO) mice on a high-fat diet (HFD) were exposed to 75 dB noise for 12 weeks to explore the effect of low-intensity noise on obesity development and the role of PPARα. 3T3-L1 cells were treated with dexamethasone (DEX) to verify the down-stream effect of hypothalamic-pituitary-adrenal (HPA) axis activation on the adipose tissues.Results The average body weight gain (BWG) of WT mice on HFD exposed to noise was inhibited by 34.6%, which was not observed in KO mice. The mass and adipocyte size of adipose tissues accounted for the above difference of BWG tendency. In WT mice on HFD, the adrenocorticotropic hormone level was increased by the noise challenge. The aggravation of fatty liver by noise exposure occurred in both mouse lines, and the transport of hepatic redundant lipid to adipose tissues were similar. The lipid metabolism in adipose tissue driven by HPA axis accorded with the BWG inhibition, validated in 3T3-L1 adipogenic stem cell model.Conclusion Chronic exposure to low-intensity noise aggravated fatty liver in both WT and KO mice. BWG inhibition was observed only in WT mice, which covered up the aggravation of fatty liver by noise exposure. Lipid metabolism in adipose tissues driven by HPA axis activation contributed to the disassociation of BWG and fatty liver development in WT mice.