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Microglial NF-κB Signaling Deficiency Protects Against Metabolic Disruptions Caused by Volatile Organic Compound via

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    Environmental benzene exposure, a common VOC, causes hyperglycemia and inflammation by affecting hypothalamic insulin resistance and neuroinflammation. Targeting IKKβ in immune cells or microglia protects against these metabolic disruptions.

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    Area of Science:

    • Environmental Science
    • Neuroscience
    • Metabolic Disease Research

    Background:

    • Benzene, a prevalent volatile organic compound (VOC), is found in smoke and linked to metabolic impairments in humans.
    • Prolonged exposure to benzene can trigger hyperglycemia and inflammation, suggesting a role in metabolic dysfunction.

    Approach:

    • Utilized a controlled exposure system and continuous glucose monitoring (CGM) in mice to study benzene's effects.
    • Investigated hypothalamic transcriptome alterations, focusing on insulin and immune response genes.
    • Examined the role of IKKβ/NF-κB signaling pathway and microglial activation.

    Key Points:

    • Benzene exposure rapidly increased blood glucose and disrupted energy homeostasis in mice.
    • Hypothalamic insulin resistance and neuroinflammation were identified as key consequences.
    • Activation of microglial transcription via the IKKβ/NF-κB pathway was observed.
    • Selective IKKβ removal in immune cells or microglia ameliorated benzene-induced effects.

    Conclusions:

    • Airborne toxicant exposure, specifically benzene, directly contributes to the onset of metabolic diseases.
    • The study elucidates a critical pathophysiological mechanism involving hypothalamic inflammation and insulin resistance.
    • Targeting the IKKβ pathway offers a potential therapeutic strategy for benzene-induced metabolic dysfunction.