Microglia Mediate Metabolic Dysfunction From Common Air Pollutants Through NF-kB Signaling

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Microglia Mediate Metabolic Dysfunction From Common Air Pollutants Through NF-kB Signaling

The prevalence of type 2 diabetes (T2D) poses a significant health challenge, yet the contribution of air pollutants to T2D epidemics remains under-studied. Several studies demonstrated a correlation between exposure to volatile organic compounds (VOCs) in indoor/outdoor environments and T2D. Here, we conducted the first meta-analysis, establishing a robust association between exposure to ben-zene, a prevalent airborne VOC, and insulin resistance in humans across all ages. We used a controlled benzene exposure system, continuous glucose monitoring approach, and indirect calorimetry in mice, to investigate the underly-ing mechanisms. Following exposure, disruptions in energy homeostasis, accompanied by modifications in the hypo-thalamic transcriptome and alterations in insulin and immune signaling, were observed exclusively in males, leading to a surge in blood glucose levels. In agreement, RNA sequencing of microglia revealed increased expression of genes associated with immu ne response and NF-kB signaling. Selective ablation of IKKb in immune cells (Cx3cr1GFPDIKK) or exclusively in microglia (Tmem119ERDIKK) in adult mice alleviated benzene-induced gliosis, restored energy homeostasis and hypothalamic gene expression, and protected against hyperglycemia. We conclude that the microglial NF-kB pathway plays a critical role in chem-ical-induced metabolic disturbances, revealing a vital pathophysiological mechanism linking exposure to airborne toxicants and the onset of metabolic diseases. © 2024 by the American Diabetes Association.

Authors : Debarba L.K.; Jayarathne H.S.M.; Stilgenbauer L.; Terra Dos Santos A.L.; Koshko L.; Scofield S.; Sullivan R.; Mandal A.; Klueh U.; Sadagurski M.

Source : American Diabetes Association Inc.