A study published in the journal JCI Insight showed that prolonged exposure to PM2.5 microparticles directly disrupts the functioning of brown adipose tissue and thereby contributes to the development of insulin resistance, obesity, and type 2 diabetes.
Experiments have shown that when exposed to PM2.5, brown fat loses its ability to efficiently process lipids and produce heat — key functions of this tissue that regulates energy metabolism. The researchers recorded changes in the expression of energy-related genes and signs of structural damage in the tissue.
Epigenetic changes were found to be the key mechanism: under the influence of pollution, the activity of brown adipose tissue genes is “reprogrammed” without changing the DNA itself. In this process, the enzymes HDAC9 and KDM2B play a crucial role, changing the epigenetic state of cells and blocking normal metabolic reactions.
When the scientists artificially inhibited the activity of HDAC9 and KDM2B, normal metabolism in brown fat was restored, demonstrating that the changes are not only descriptive but also reversible when these enzymes are affected. Therefore, HDAC9 and KDM2B are potential therapeutic targets to prevent metabolic disorders caused by air pollution.
The head of the study, Professor Francesco Paneni, emphasized that the results explain the direct connection between air quality and human metabolism and open up new avenues for the prevention and treatment of metabolic disorders.
These findings have important public health implications: tackling air pollution is becoming not only an environmental but also a metabolic priority. The development of drugs that target HDAC9 or KDM2B could complement PM2.5 exposure reduction measures and help reduce the burden of insulin resistance, obesity, and type 2 diabetes at a population scale.
