Axe intestin-cerveau et régulation de la satiété chez l'obèse : étude de l'origine de l'endotoxémie métabolique et de son rôle sur la physiologie du nerf vague dans un modèle d'obésité induite par un régime occidental chez le rat

Abstract : A real public health issue, obesity and its associated metabolic and behavioral disorders are the consequences of a state of low grade chronic inflammation that might originate from the presence in host plasma of gut-derived bacteria components, lipopolysaccharides (LPS). This present state is called metabolic endotoxemia. The first aim of my thesis was to understand why, in diet-induced obesity (DIO), LPS initially contained in the gut lumen, are able to cross the intestine and enter into the circulatory system. My second aim was to investigate the effect of gut microbiota composition and LPS on the satiety regulation by the vagus nerve, the main communication pathway between the gut and the brain. To answer these questions, we have mainly used a DIO rat model.We showed that consumption of WD induced a loss of ileal barrier function characterized by a reduction in mucosal defenses associated to elevated LPS permeability. Obesity is also characterized by an alteration in feeding behavior including a decreased sensitivity to intestinal satiety signals. We showed that neither obesity nor the lipid percentage of the diet triggers loss of sensitivity to satiety signals but that gut microbiota alterations could rather be the main driver. Hence, metabolic endotoxemia could result from an increased transepithelial passage of LPS, which once spread in the blood could reach, among other things, the vagus nerve where they could disrupt intestinal signals of satiety.
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Mathilde Guerville. Axe intestin-cerveau et régulation de la satiété chez l'obèse : étude de l'origine de l'endotoxémie métabolique et de son rôle sur la physiologie du nerf vague dans un modèle d'obésité induite par un régime occidental chez le rat. Science des productions animales. Agrocampus Ouest, 2016. Français. ⟨NNT : 2016NSARB288⟩. ⟨tel-01636622⟩

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