Researchers exposed laboratory mice to either filtered air or concentrated PM2.5 particles, tiny pollutants less than 2.5 micrometers in diameter for six hours a day, five days a week, over 24 weeks. This experiment was designed to simulate chronic urban pollution exposure in humans. The team focused on brown fat, a specialized form of adipose tissue critical for regulating body heat and glucose metabolism.
After nearly five months, mice exposed to PM2.5 showed clear signs of metabolic dysfunction, including insulin resistance and altered brown fat activity. “In particular, we found that the expression of important genes in brown adipose tissue which regulate its ability to produce heat, process lipids and handle oxidative stress were disturbed,” said Francesco Paneni, professor at the Center for Translational and Experimental Cardiology of the University of Zurich. The affected mice also exhibited increased fat accumulation, tissue damage, and early signs of fibrosis.
To understand the underlying biological mechanisms, the scientists examined changes in gene regulation within brown fat cells. They discovered that air pollution caused significant epigenetic modifications—particularly in DNA methylation and chromatin structure. Two key enzymes, HDAC9 and KDM2B, were found to be responsible for these changes by modifying histone proteins, which affected how genes were activated or silenced.
The findings present new evidence that air pollution can be a driver of metabolic disease by altering gene function in fat cells.
Reference: Palanivel R, Dazard JE, Park B, Costantino S, Moorthy ST, Vergara-Martel A, Cara EA, Edwards-Glenn J, Biswal S, Chen LC, Jain MK. Air pollution modulates brown adipose tissue function through epigenetic regulation by HDAC9 and KDM2B. JCI Insight. 2025 Sep 23;10(18).
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