Since insulin compounds can restore some metabolic parameters and lipid profile alterations of the diabetic rat heart, we investigated whether these beneficial effects extend to diabetic rat cardiac dysfunctions. Twenty-four male Wistar albino rats, 6 months of age with an average body weight of 250-320 g, were divided randomly into three groups, each consisting of eight rats: control-group (C) rats were fed with standard rat nutrient and water; diabetic-group (D) rats were treated with a single intramuscular injection of streptozotocin (STZ, 45 mg/kg), dissolved in 0.01 M sodium citrate, pH adjusted to 4.5; and insulin-treated diabetic group (D + INS) rats were treated with subcutaneous injections of 1 IU/l insulin (INS) twice a day after a single intramuscular injection of STZ (45 mg/kg). Treatment of D rats with INS caused a time-dependent decrease in blood glucose. We found that the lipid profile and HbA(1c) levels in the D + INS group reached the values of control rats at the end of the treatment period. Contraction force in group D was compared with values from groups C and D + INS (p < 0.05). Values were obtained at a muscle contraction and relaxation time of milliseconds, with contraction time in D compared to C and D compared to D + INS and C (p < 0.05). Rate-dependent changes in action potential configuration in left ventricular papillary muscle obtained from 8-week control, STZ-treated D and D + INS rats showed significant membrane potential changes between C and STZ-treated D animals. Action potential amplitude showed significant changes between matched D + INS and STZ-treated D animals. Depolarization time showed significant changes between C and STZ-treated D animals and between the D + INS and D groups. Half-repolarization time showed significant changes between D + INS and STZ-treated D animals and compared to the D and C groups. Our data suggest that the beneficial effects of insulin treatment on the mechanical and electrical activities of the diabetic rat heart appear to be due to restoration of the diminished K+ currents, partially related to the restoration of hyperglycemia.