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Air pollution tied to obesity and diabetes

Air pollution could make people more prone to obesity and diabetes, according to a new international study led by scientists at the University of Zurich (UZH) and Case Western Reserve University.

The researchers found that long-term exposure to fine air pollution can disrupt the body’s metabolism by interfering with how our ‘good’ fat works.

In their study, mice were exposed to either clean air, filtered air or air containing concentrated levels of PM2.5 for six hours a day, five days a week, over nearly six months – similar to chronic exposure levels in large cities.

At the end of the study, mice exposed to the polluted air showed clear signs of metabolic problems. Their bodies were less able to regulate blood sugar and they began to store more fat. Scientists found that the brown fat, which normally burns calories and helps control body temperature, wasn’t working properly.

Professor Francesco Paneni, one of the study’s lead authors, said: ‘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.

‘These changes were accompanied by increased fat accumulation and signs of tissue damage and fibrosis within the tissue.’

Digging deeper, the team discovered that pollution caused chemical changes in the mice’s DNA – not mutations, but epigenetic changes, which affect how genes are turned on or off.

Two enzymes, HDAC9 and KDM2B, appeared to play a central role in this process by altering the structure of DNA and silencing important metabolic genes. When these enzymes were blocked in experiments, the brown fat began working normally again.

The findings suggest that long-term air pollution exposure could directly contribute to the development of insulin resistance and metabolic disorders such as type 2 diabetes.

Paneni added: ‘Our findings help explain how environmental pollutants like PM2.5 contribute to the development of insulin resistance and metabolic disease, and they point to potential new targets for prevention or treatment.’

The full research can be read here.

Paul Day
Paul is the editor of Public Sector News.
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