Air pollution may increase the risk of diabetes by disrupting how the body regulates metabolism, according to new research by scientists from the University of Zurich and Case Western Reserve University.
The study, published in JCI Insight, reveals that fine particulate matter known as PM2.5 can alter brown fat function, an organ responsible for burning energy and controlling blood sugar, pushing the body toward insulin resistance and metabolic disease.
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Researchers exposed mice to city-like concentrations of PM2.5 for six hours a day, five days a week, over 24 weeks.
They discovered that the polluted air impaired insulin sensitivity and triggered gene expression changes in brown fat, reducing its ability to produce heat, process lipids, and manage oxidative stress.
These molecular disruptions led to fat buildup, tissue damage, and fibrosis, indicating declining metabolic health.
Further analysis revealed that pollution caused sweeping epigenetic shifts, changes that modify gene activity without altering DNA.
Two key enzymes, HDAC9 and KDM2B, were identified as culprits that suppress normal brown fat function when overactive.
Suppressing these enzymes experimentally restored brown fat activity, while enhancing them worsened the metabolic decline.
Scientists warn that PM2.5, produced mainly from traffic, industrial emissions, and wildfire smoke, poses a significant public health threat.
The findings highlight the need for stricter air quality standards and cleaner transportation systems to reduce pollution-linked diseases.
Researchers suggest that therapies targeting brown fat’s gene regulation or lifestyle changes that enhance brown fat activity could help mitigate the effects of pollution.
They also call for further studies to determine whether these mechanisms occur in humans and whether the changes are reversible.
The research underscores that clean air is essential not only for lung and heart health but also for maintaining the body’s metabolic balance. Nature News
