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<dc:title xml:lang="fr">Rôle de l'hyperactivité sympathique dans la physiopathologie du syndrome métabolique</dc:title>
<dcterms:alternative xml:lang="en">Involvement of sympathetic hyperactivity in the pathophysiology of the metabolic syndrome</dcterms:alternative>
<dc:subject xml:lang="fr">Hyperactivité sympathique</dc:subject>
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<dc:subject xml:lang="fr">Syndrome métabolique</dc:subject>
<dc:subject xml:lang="fr">Intolérance au glucose</dc:subject>
<dc:subject xml:lang="fr">Insulinosécrétion</dc:subject>
<dc:subject xml:lang="en">Sympathetic hyperactivity</dc:subject>
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<dc:subject xml:lang="en">Metabolic syndrome</dc:subject>
<dc:subject xml:lang="en">Glucose intolerance</dc:subject>
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<tef:elementdEntree autoriteExterne="028090942" autoriteSource="Sudoc">Troubles du métabolisme des glucides</tef:elementdEntree>
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<dcterms:abstract xml:lang="fr">L’existence d’une relation entre les troubles cardio-métaboliques composant le syndrome métabolique et une hyperactivité sympathique est bien admise dans la littérature sans que la relation causale entre ces deux entités soit clairement définie. Nos travaux sur un modèle murin d’hyperactivité sympathique constitutive (délétion partielle et/ou complète du transporteur de recapture de la noradrénaline) ont permis de mettre en évidence le rôle de celle-ci dans le développement de troubles glucidiques : 1) Une augmentation de l’activité sympathique est un facteur suffisant pour le développement de troubles glucidiques précoces associant une intolérance au glucose à une hyperinsulinémie basale sans hyperglycémie. 2) Ces désordres seraient dus à un retard de sécrétion d’insuline en réponse au glucose, probablement consécutif à une sous-expression du transporteur GLUT2. Ces résultats montrent que l’hyperactivité sympathique chronique pourrait constituer un facteur pronostic permettant le diagnostic précoce de patients à risque de développer des troubles de l’homéostasie glucidique et ouvre des perspectives dans le traitement du diabète de type 2.</dcterms:abstract>
<dcterms:abstract xml:lang="en">Several studies have established an association between cardiometabolic disorders composing the metabolic syndrome and sympathetic hyperactivity. The causal relationship is however not clearly defined. Our work on a murine model of constitutive sympathetic hyperactivity (partial and / or complete deletion of the norepinephrine reuptake transporter) highlights its role in the development of carbohydrate disorders: 1) An increase in the sympathetic activity is a sufficient factor for early carbohydrate disorders associating glucose intolerance with basal hyperinsulinemia without hyperglycemia. 2) These disorder are thought to be due to a delay in insulin secretion in response to glucose stimulation, probably consecutive to a decreased expression of the GLUT2 transporter. These results show that chronic sympathetic hyperactivity may constitute a prognostic factor allowing the early diagnosis of patients at risk to develop glucose homeostasis disorders and opens perspectives in the treatment of type 2 diabetes mellitus.</dcterms:abstract>
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