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Insulin resistance: A new consequence of altered carotid body chemoreflex?

      The carotid bodies (CBs) are arterial chemoreceptors that respond to hypoxia by increasing action potential frequency in their sensory nerve, the carotid sinus nerve (CSN), increasing minute ventilation and activating the sympathetic nervous system. Besides its role in the control of ventilation, the CB has been proposed as a metabolic sensor implicated in the control of energy homeostasis. We have recently described that CB overactivation is the pathophysiological mechanism involved in the etiology of insulin resistance and hypertension, core central metabolic and hemodynamic disturbances of highly prevalent diseases like type 2 diabetes and the metabolic syndrome. Additionally, we have demonstrated that CB activity is increased in insulin resistant animal models and our lab has shown that surgical ablation of the CSN prevents the development of insulin resistance and hypertension induced by hypercaloric diets. Herein, we tested if established insulin resistance and hypertension, may also be reversed by the abolishment of CB activity, through CSN denervation, in diet-induced animal models of metabolic diseases. Additionally, the mechanism behind the effect of CSN resection on metabolism was investigated. We demonstrated that CSN denervation re-established insulin sensitivity, normoglycemia and normoinsulinemia and lowered mean arterial pressure in animal models of insulin resistance and hypertension. Additionally, we showed that CSN resection restores insulin sensitivity in diet-induced insulin resistant rats through a repair of insulin signalling pathways in adipose tissue and skeletal muscle. We propose that the modulation of CB activity can be a therapeutic approach for the treatment of metabolic diseases. Supported by: EXPL/NEU-SCC/2183/2013, Glaxo Smith Kline Bioelectronics Exploratory Funding. MJ Ribeiro by SFR/BD/88983/2012. JF Sacramento by PD/BD/105890/2014.
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