The carotid bodies (CB) are peripheral chemoreceptors that classically respond to hypoxia, hypercapnia and acidosis. When activated CB chemoreceptor cells release neurotransmitters that increase chemosensory activity in the carotid sinus nerve (CSN), causing hyperventilation and activation of the sympathoadrenal system (Gonzalez et al. 1994; Marshall et al. 1994). 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 (Pardal and Lopez-Barneo, 2002; Koyama et al. 2000). Since, increased sympathetic activity is a well-known pathophysiological mechanism in IR and hypertension (HT) we hypothesize that overactivation of CB can contribute to the development of IR and HT. Therefore, the objective of this study was to investigate if CB activity is increased in IR and HT animal models. Experiments were performed in 3 months Wistar rats (200-420 g) of both sexes. anaesthetized with pentobarbitone (60mg/Kg, ip). Two diet-induced IR and HT animal models were used: the rat submitted to a high-fat (HF) diet, a model that combines obesity, IR and HT and the rat submitted to a high-sucrose (HSu) diet, a lean model of combined IR and HT. CB activity was assessed through the evaluation of: in vivo ventilatory responses by measuring spontaneous ventilation and in response to ischemic hypoxia and in vitro by monitoring catecholamines release in basal conditions and in response to acute hypoxia (5%O2) and the expression of tyrosine hydroxylase. We have observed that spontaneous ventilation as well as ventilation in response to ischemic hypoxia (assessed as the increase in ventilation produced by common carotid artery occlusions for periods of 5, 10 and 15 seconds) were increased in HF and HSu animals, with a more pronounced effect in HF animals. Surgical CSN cut completely abolished the increases in ventilation induced by the diets, showing that these effects are mediated by the CB. Basal release of dopamine was not significantly modified by hypercaloric diets, however the release induced by hypoxia (5%O2) was increased 3.15 and 2.12 fold in HF and HSu rat models, respectively. Also, CBs weight was significantly increased by 36.71% and 27.13% in HF and HSu models, respectively, as well as tyrosine hydroxylase expression, the rating enzyme for catecholamine biosynthesis, that increased by 64.4% in HF (p<0.01) and 30.8% in HSu animals (p=0.12). In conclusion, we demonstrated for the first time that CB activity is increased in diet-induced animal models of IR and HT suggesting that CB is involved in the development of IR and HT. Additionally, the more pronounced increases in spontaneous ventilation and in ischemic hypoxia induced-hyperventilation observed in HF animals suggest that these animals hold a higher degree of CB activation.