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Objectives Infections, cancer and systemic inflammation elicit anorexia. Despite the medical significance of this phenomenon, the question of how peripheral inflammatory mediators affect the central regulation of food intake is incompletely understood. Therefore, we have investigated the sickness behavior induced by the prototypical inflammatory mediator IL-1β. Methods IL-1β was injected intravenously. To interfere with IL-1β signaling we deleted the essential modulator of NF-κB signaling (Nemo) in astrocytes and tanycytes. Results Syst
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