Long-term exposure to particulate matter can impair the healthy metabolism of mice by disrupting the function of brown adipose tissue. This leads to insulin resistance and potentially metabolic diseases such as type 2 diabetes. A study by the University of Zurich (UZH) and Case Western Reserve University in Cleveland sheds light on the underlying epigenetic mechanisms.

The researchers led by Francesco Paneni from UZH and Sanjay Rajagopalan from Cleveland investigated the effects of PM2.5 particles, which are smaller than 2.5 micrometers and can penetrate deep into the lungs. Laboratory mice were exposed to either filtered air or concentrated particulate matter for six hours five days a week for 24 weeks to mimic urban pollution.

After about five months, the exposed mice showed reduced insulin sensitivity and changes in brown adipose tissue, which is responsible for heat production and calorie burning. Genes for heat generation, fat processing and oxidative stress were affected, which led to fat accumulation, tissue damage and increased connective tissue.

The study identified epigenetic changes in the DNA regulation of fat cells, including altered methyl group patterns and chromatin remodeling, that affect gene activity without altering the genetic code. Two enzymes, HDAC9 and KDM2B, play a central role: they bind to DNA regions and reduce promoting marks. Experimental suppression of the enzymes improved adipose tissue function, while increasing it further worsened.

The results indicate that particulate matter contributes to the development of metabolic disorders via these mechanisms and could offer new targets for prevention or therapy. There is increasing evidence that air pollution not only damages the lungs and heart, but also promotes metabolic diseases.

Original Paper:

JCI Insight – Air pollution modulates brown adipose tissue function through epigenetic regulation by HDAC9 and KDM2B

Editor: X-Press Journalistenbüro GbR

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