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https://www.selleckchem.com/products/loxo-195.html 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 Systemic IL-1β increased the activity of the transcription factor NF-κB in tanycytes of the mediobasal hypothalamus (MBH). By activating NF-κB signaling, IL-1β induced the expression of cyclooxygenase-2 (Cox-2) and stimulated the release of the anorexigenic prostaglandin E2 (PGE2) from tanycytes. When we deleted Nemo in astrocytes and tanycytes, the IL-1β-induced anorexia was alleviated whereas the fever and lethargy response were unchanged. Similar results were obtained after selective deletion of Nemo exclusively in tanycytes. Conclusions Tanycytes form the brain barrier that mediates the anorexic effect of systemic inflammation in the hypothalamus.Objectives Elevated plasma glucagon is an early symptom of diabetes, occurring in subjects with impaired glucose regulation. Here we explored alpha-cell function in female mice fed a high fat diet (HFD) - a widely used mouse model of pre-diabetes. Methods We fed female mice expressing the Ca2+ indicator GCaMP3 specifically in alpha-cells a HFD or control (CTL) diet. We then conducted in vivo phenotyping of these mice, as well as experiments on isolated (ex vivo) islets and in the in situ perfused pancreas. Results In vivo, HFD-fed mice exhibited increased fed plasma glucagon levels and a reduced response to elevations in plasma glucose. Glucagon secretion from isolated islets and in the perfused mouse pancreas was elevated under both hypo- an

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