Introduction:  Metabolic diseases, like type 2 diabetes (T2D) and obesity are highly incident diseases worldwide caused in part by hypercaloric diets [1]. Recently, we demonstrated that the activity of the carotid body (CB) is increased in prediabetes and T2D animals [2], and in prediabetic patients [3] and that the resection of the carotid sinus nerve (CSN), the nerve that links CB to the brain, prevented and reversed the metabolic alterations induced by hypercaloric diets in rats [2,4]. The nucleus of the tractus solitarius (NTS) is an integrative center of CSN signals distributing information to nucleus within other regions of the brain like the hypothalamus [5]. We propose to discriminate the type of integration and distribution of CSN metabolic signals to understand the brain regions involved in the CB-dependent metabolic control and complete the circuit between CB-brain-peripheral tissues in the scenario of metabolic disorders. Material & Methods:  Cryopreserved brains of male Wistar sham vs CSN-transected control and HF rats (19 weeks diet treatment) were cut in coronal sections (40um) following the coordinates from bregma to englobe NTS region from caudal (-14mm), to medial (-12,5mm) and rostral (-11mm) regions and 2 important regions of the hypothalamus the paraventricular nucleus (PVN) and the arcuate (ARC). Free-floating immunofluorescence for delta-FosB, an early gene used to measure brain activity was performed. Slices were visualized in a confocal microscope and images were used to count the fluorescence intensity correspondent to delta-FosB staining. Experiments followed the European Union Directive for Protection of Vertebrates Used for Experimental and Other Scientific Ends (2010/63/EU) and were approved by the NOVA Medical School Ethics Committee and the Portuguese Authority for Animal Health. Data was analyzed and differences were calculated using One-Way ANOVA with Turkey’s multiple comparison test and considered significantly different with p-values < 0.05. Results:  Delta-FosB relative fluorescence was not altered in control animals undergoing CSN denervation in all NTS regions. Also, HF diet did not promote any alteration in delta-FosB relative fluorescence in all NTS regions. However, CSN denervation in HF animals promoted a significant decrease in delta-FosB relative fluorescence in the rostral (ctl=100%±14.4% vs. HF+Den= 59.5%±16.3%; p=0.037) and medial regions (ctl=100%±2.7% vs HF+Den=86%±3.3%; p=0.0046) of the NTS, without alterations in the caudal region. HF diet did not change delta-FosB fluorescence in the sub-region of PVN and ARC at -1.8mm from bregma, but CSN denervation in control and HF animals promoted an increase in delta-FosB fluorescence in this sub-region of PVN (ctl=100%±10.1%, ctl+Den=234.8%±80.2% (p=0.021); HF=105.4%±34.3% vs HF+DEN=171.9%±4.3, p=0.032) without alterations in the ARC on this coordinate. At -2.16mm the HF diet promoted an increase in delta-FosB staining in the PVN that was reverted by CSN denervation (ctl=100%±0.0% vs HF=150.2%±5.1%, p=0.005; HF vs HF+DEN=85.3%±9.6%, p=0.003) again without alterations the ARC. Conclusions: We can conclude that the signals from CB integrated in the NTS affect the hypothalamus, particularly the PVN. Further experiments must be done to explore neuronal populations within these regions of the hypothalamus that are modulated by CB in states of dysmetabolism.