Ecotoxicology and environmental safetySep 24, 2026

The role of Per2 in liver fat production caused by long-term noise through PPARγ and SREBP-1 pathways

Circadian Biology Weekly Brief ↗PubMed ↗DOI ↗

Updated Sep 25, 2026

Abstract

Thirty days of noise exposure in mice led to increased hepatic lipid accumulation.

Chronic noise exposure is linked to changes in liver fat metabolism without impacting body weight or food intake.
The noise exposure disrupted the timing of liver lipid metabolism, resulting in increased triglyceride levels and altered expression of genes related to fat metabolism.
A total of 613 genes exhibited changes in rhythmic expression related to lipid metabolism and circadian rhythms, with the core clock gene Per2 identified as a central player.
Altered expression of the PER2 protein was connected to changes in the signaling pathways involving PPARγ and SREBP-1.
Knocking out the Per2 gene reduced the liver lipid abnormalities associated with noise exposure and lowered the expression of Srebf1 and levels of PPARγ/SREBP-1 proteins.

Simplified

Chronic noise exposure is increasingly recognized as an environmental risk factor for metabolic disorders; however, whether and how circadian dysregulation contributes to noise-induced hepatic lipid abnormalities remains unclear. Here, we investigated the role of circadian regulation in chronic noise-induced hepatic lipid metabolic alterations using transcriptomic, metabolomic, and genetic approaches. Thirty-day noise exposure in C57BL/6 J mice induced hepatic lipid accumulation and mild histopathological changes without affecting body weight or food intake. Noise exposure altered the temporal regulation of hepatic lipid metabolism, characterized by increased hepatic triglyceride accumulation and altered expression of fatty acid metabolic genes, including Fads2 and Elovl6. Transcriptomic profiling identified 613 genes with altered rhythmic expression patterns enriched in lipid metabolic and circadian-related pathways, with the core clock gene Per2 emerging as a candidate hub gene. qPCR-based circadian analysis and time-resolved protein validation demonstrated altered PER2 expression accompanied by changes in PPARγ/SREBP-1 signaling components. Untargeted metabolomics further revealed noise-associated lipogenic metabolic alterations, which were partially attenuated by Per2 deletion. Mechanistically, Per2 knockout alleviated noise-associated hepatic lipid abnormalities and reduced the induction of Srebf1 expression and PPARγ/SREBP-1 protein abundance. Collectively, these findings identify Per2 as an important circadian regulator involved in noise-induced hepatic lipogenic responses and provide new insights into the link between environmental stress, circadian regulation, and metabolic dysfunction.

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The role of Per2 in liver fat production caused by long-term noise through PPARγ and SREBP-1 pathways

Abstract

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