The aim of this work was to evaluate the ATP sensitive potassium current in type 2 diabetic animals (db/db) and cardiac protein expression of these channels and channel regulatory protein SUR-2A. Fifteen-week-old male C57BL/KsJ-db (db/db) mice and their control littermates (-/-) were used. All experiments were carried out according to European Union Council Directives (86/609/EEC) for the care of laboratory animals. Mice were weighed and anesthetized with sodium pentobarbital (100 mg/kg i.p.) and the heart was quickly removed and weighed as described (Pereira L et al. 2006). Ventricular Cardiac cells were enzymatically isolated (as described by Lauton-Santos S et al. 2007) from controls (n=16) and diabetic (db/db,n=16) and Whole-cell voltage clamp was performed to measure ATP-sensitive K current (IKATP). The holding potential was set at -80 mV and depolarization from -40 mV to +50 mV in 10 mV steps were applied every 20 ms. Ventricular Cardiac cells from controls (n=5) and diabetic (db/db,n=8) were processed to extract protein and submitted to gel electrophoresis and then subjected to western blot protocol as described by Primola-Gomes TN et al. (2009). Specific antibody (anti-KIR 6.2, SUR-2A and anti-GAPDH from Santa Cruz Biotechnology and Affinity BioReagents) and secondary antibody (SIGMA, Sto Louis) were used. The signal was detected using ECL kit (Amersham, IL, USA). The images generated were quantitatively analyzed using KODAK software. We found a significant increase (30%) in the ATP sensitive potassium current and also in the protein expression level of KATP channels (three times bigger in db/db animals when compared with control animals) and no differences between SUR-2A expression was detected. We conclude that cardiac KATP sensitive current is increased in diabetic mice.