**6. Conclusion**

Diabetes is not merely a disease of impaired insulin sensitivity or insulin release, but may be a global metabolic dysfunction, including, among others, the collapse of the mitochondrial energy system. The role of the mitochondria in the metabolism associated with the pathophysiology of diabetes seems unique, mainly because a generation of ROS (which seem a natural part of mitochondrial physiology) constitutes a major treat in the development of diabetic sequelae. ROS play the central role in mediating various metabolic defects associated with the diabetic state. Therefore, inhibition of ROS production and/or enhancement of ROS scavenging will prove to be beneficial therapies. Hyperglycaemia elicits an increased ROS production, presumably from the mitochondrial respiratory chain. An important challenge for future research is to determine whether strategies aimed to improving mitochondrial functionality by using agents with anti-diabetic properties might have therapeutic potential in the treatment of diabetes. On the other hand, the better understanding of mitochondrial biology is still needed to facilitate the judicious selection and development of compounds/agents, which could be used as "mitochondrial drugs". Further studies are certainly required to better understand how these novel compounds and mitochondria may interact with each other, and how our understanding of such interaction might be utilized for the impaired mitochondrial functioning in the presence of diabetes. These investigations should also determine, which genetic, environmental, pharmacological and nutritional factors are possibly involved in an individual patient's susceptibility and, which treatments can be used safely in those patients, who suffer from heavy diabetes and are crushed by the burden of advanced long-term complications.
