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Obesity and excessive dietary consumption promote an inflammatory state in peripheral metabolic tissues driven by ingress and activation of immune cells. Likewise, the central nervous system responds to high fat and sugar-rich diets with rapid upregulation of the master inflammatory NF-κB pathway in important brain regions including the hypothalamus, a critical site of energy homeostasis regulation. Thus, identifying mechanisms that regulate the hypothalamic inflammatory process can advance our understanding of obesity pathogenesis and assist with development of new treatment targets.

Recent evidence suggests that neuronal inflammation may be a downstream event during diet-induced obesity (DIO), with the recruitment and activation of hypothalamic glial cells being a more proximal response to high fat diet (HFD) exposure. While several studies have implicated microglia in the generation of diet-induced inflammatory signals and metabolic dysfunction, a similar role for astrocytes remains unclear. To address this, Douglass et al. developed a mouse model with an inducible astrocyte-specific deletion of IKKβ. Using this approach, they demonstrate that reduction of astrocyte inflammatory signaling protects mice from HFD-induced hypothalamic inflammation and reduces susceptibility to DIO and glucose intolerance. These results highlight the important role of non-neuronal cells in obesity pathogenesis and suggest the possibility of new cellular targets for therapy.

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In this section authors briefly report on their work recently published in Molecular Metabolism.

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Brandon L Roberts, Baylin Bennett
Oregon National Primate Research Center, Beaverton, Oregon, USA
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