Overactivity of the sympathetic nervous system (SNS) is associated to several cardiovascular and metabolic dysfunctions, such as hypertension and insulin resistance. Indirect biochemical measurements and surgical manipulations have provided preliminary evidences about a crucial role of the Carotid Sinus Nerve (CSN) in generating the SNS overactivity. However, CSN and SNS neural activities and their interplay have not been yet characterized in healthy and pathological conditions. Understanding this relationship is key for the development of electroceutical approaches to deliver therapeutic neuromodulation to the autonomic nervous system and restore insulin sensitivity. Here we show that early type 2 diabetes rats present a high frequency shift in both CSN and SNS neural activities with respect to control animals. This feature could be an important neural signature characterizing type 2 diabetes. Moreover, we show that CSN resection in early type 2 diabetes rats abolishes SNS high frequency shift confirming that normal SNS activity and insulin sensitivity may be recovered by CSN activity suppression. These findings shed new light on the pathological neural changes within the autonomic nervous system in type 2 diabetes. Moreover, they pave the way for electrical monitoring of the metabolic state of diabetic patients, a key first step for the development of electroceutical therapies.