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Astiz M.,and bHospital Infantil Universitario Nino Jesus | Pernia O.,and bHospital Infantil Universitario Nino Jesus | Barrios V.,and bHospital Infantil Universitario Nino Jesus | Garcia-Segura L.M.,and bHospital Infantil Universitario Nino Jesus | Diz-Chaves Y.,and bHospital Infantil Universitario Nino Jesus
Neuroendocrinology | Year: 2016

Obesity is associated with increased fever and sickness behavior in response to infection. The hypothalamic-pituitary-adrenal (HPA) axis plays a key role in the reaction to immune stimuli. Bacterial infection, or bacterial lipopolysaccharide (LPS), induces the expression of peripheral cytokines that stimulate the hypothalamus and the hippocampus and activate the HPA axis. In this study, we explored whether the hypothalamic and hippocampal responses to infection is altered during the development of diet-induced obesity. Male mice were exposed to high fat diet (HFD) or low fat diet (LFD) for 15 days. They were then administered a single intraperitoneal injection of bacterial lipopolysaccharide (LPS) or vehicle and sacrificed 24 h later. LPS increased circulating levels of insulin and leptin, but only in LFD animals. LPS induced a significant decrease in hypothalamic corticotrophin-releasing hormone (CRH) and glucocortioid receptor (GR) mRNA levels in LFD animals and the opposite effect in HFD fed mice. LPS increased the hypothalamic expression of molecules involved in the leptin signaling pathway (SOCS3, STAT3), NFκB pathway members, inflammatory mediators (TNFα, IL6) and glial proliferation markers (Emr1 and CD68) in LFD animals. These effects were dampened in HFD-fed mice. In contrast, the hippocampal responses to LPS were largely insensitive by HFD. These results suggest that HFD feeding reduced the inflammatory response induced by LPS in the hypothalamus, but not in the hippocampus. © 2016 S. Karger AG, Basel

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