Abstract
Air pollution is involved in several processes harmful to health. PM2,5 is the most associated with the induction of chronic inflammation. Hypothalamus regulates the energy homeostasis thought metabolic, neural and hormonal signals. Leptin signaling participates in this process, and hypothalamic inflammation may induce leptin resistance. TLR4 is an innate immune receptor capable of triggering subclinical inflammation, and one of its agonists is LPS, which is known be present in the PM2.5 composition. Polluted C57 mice had increased adiposity due to hyperphagia and lower energy expenditure, caused by leptin resistance. The TLR4 gene expression was elevated in the hypothalamus of polluted C57. The TLR4 deletion protected the animal from obesity, glucose intolerance, and leptin resistance when exposed to PM2.5. Together, these results suggest that air pollution induces hypothalamic leptin resistance by the activation of inflammatory pathways, probably involving TLR4.
Highlights
Exposure to air pollution has unfavorable cardiometabolic effects contributing to the increase in mortality
These results suggest that air pollution induces hypothalamic leptin resistance by the activation of inflammatory pathways, probably involving toll-like receptor 4 (TLR4)
TLR4 gene expression levels were elevated in the hypothalamus of polluted C57BL/6J mice (C57) mice
Summary
Exposure to air pollution has unfavorable cardiometabolic effects contributing to the increase in mortality. AIR POLLUTION PARTICIPATES IN THE GENESIS OF OBESITY THROUGH THE ACTIVATION OF HYPOTHALAMIC TLR4 Leptin signaling participates in this process, and hypothalamic inflammation may induce leptin resistance.
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