Diabetes and its chronic complications still represent a great clinical problem, despite improvements made in the diagnosis and treatment of the disease. People with diabetes have a much higher risk of impaired brain function and psychiatric disorders. Neurotrophins are factors that protect neuronal tissue and improve the function of the central nervous system, and among them is brain-derived neurotrophic factor (BDNF). The level and function of BDNF in diabetes seems to be disturbed by and connected with the presence of insulin resistance. On the other hand, there is evidence for the highly beneficial impact of physical activity on brain function and BDNF level. However, it is not clear if this protective phenomenon works in the presence of diabetes. In this review, we summarize the current available research on this topic and find that the results of published studies are ambiguous.

Type 1 diabetes mellitus is a disease involving changes to energy metabolism. Chronic hyperglycemia is a major cause of diabetes complications. Hyperglycemia induces mechanisms that generate the excessive production of reactive oxygen species, leading to the development of oxidative stress. Studies with animal models have indicated the involvement of mitochondrial dysfunction in the pathogenesis of diabetic cardiomyopathy. In the current review, we aimed to collect scientific reports linking disorders in mitochondrial functioning with the development of diabetic cardiomyopathy in type 1 diabetes mellitus. We also aimed to present therapeutic approaches counteracting the development of mitochondrial dysfunction and diabetic cardiomyopathy in type 1 diabetes mellitus.