Increased sympathetic activity is a well-known pathophysiological mechanism in insulin resistance (IR) and hypertension (HT). The carotid bodies (CB) are peripheral chemoreceptors that classically respond to hypoxia by increasing chemosensory activity in the carotid sinus nerve (CSN), causing hyperventilation and activation of the sympathoadrenal system. Besides its role in the control of ventilation, the CB has been proposed as a glucose sensor being implicated in the control of energy homeostasis. However, to date no studies have anticipated its role in the development of IR. Herein we propose that CB overstimulation is involved in the aetiology of IR and HT, core metabolic and hemodynamic disturbances of highly prevalent diseases like the metabolic syndrome, type 2 diabetes and obstructive sleep apnoea. We demonstrated CB activity is increased in IR animal models and that CSN resection prevents CB-overactivation and diet-induced IR and HT. Moreover we showed that insulin triggers CB, highlighting a new role for hyperinsulinemia as a stimulus for CB-overactivation. We propose that CB is implicated in the pathogenesis of metabolic and hemodynamic disturbances through sympathoadrenal overactivation and may represent a novel therapeutic target in these diseases.