A growing body of evidence has indicated that altered mitochondrial function may be involved in mechanism for the development of diabetic complications. Thus, we investigated whether animal model of diabetes induced by alloxan alters energy metabolism parameters. Wistar rats received one single injection of alloxan (250 mg/kg) and after 15 days we evaluated mitochondrial respiratory chain complexes I, II, II-III and IV, creatine kinase and citrate synthase activities in prefrontal cortex, hippocampus and striatum. We observed that animal model of diabetes induced by alloxan increased complexes I and IV activities in hippocampus, complexes II and II-III activities in prefrontal cortex and striatum and complex IV in prefrontal cortex; however decreased complex IV activity in striatum. Moreover, diabetes rats decreased creatine kinase activity in striatum and increased citrate synthase activity in hippocampus. In conclusion, this study indicates that the alteration in mitochondrial function is probably involved in the pathophysiology of diabetes.