diabetic encephalopathy,mitochondrial function and exercise

Background and Aim : Diabetic encephalopathy (DE) is a chronic complication of diabetes mellitus that affects the central nervous system (CNS) and is characterized by cognitive impairment in the absence of any other predisposing factors. Mitochondrial function has different implications for diabetes in different cells and tissues, this is why it carries the potential for targeting mitochondria in the therapy of diabetes. exercise remains the most potent behavioral therapeutic approach for the improvement of mitochondrial health, not only in muscle, but potentially also in other tissues such as brain and CNS. Therefore in this study we first showed mitochondrial malfunction fallowing diabetic encephalopathy(diabetes induced cognitive impairment) in rat hippocampus and then compared the effect of insulin vs exercise on its improvement.Methods : 48 male wistar rats ,weighting 200-250 gr, living in standard animal house condition we randomly selected. rats were divided into four groups: diabetes+saline, diabetes+i nsulin ,diabetes+exercise or intact .diabetes was induced by single IP injection of STZ 60 mg/kg .diabetic encephalopathy was confirmed 8 weeks fallowing diabetes induction,by impairmed step throgh latency,spontaneous alternation and EPM tests .At the end of 8th week,mitochondrial membrane potential and its function was examined by rhodamine 123 coloring.Results : our results showed improvement of learning and spacial memory and anxiety in both diabetes+exercise(P<0.01) and diabetes+insulin(p<0.05) groups, compared with saline +diabetes group. mitochondrial membrane potential showed better improvement in exercise group compared with insulin taking diabetes group(P<0.001 VS P<0.05).Conclusion : our findings showed although insulin is the choice therapy of T1DM,but impaired cognitive function induced by abnormal hippocampal function and mitochondrial membrane potential in diabetic encephalopathy is more responsive to exercise compared with insulin. Regular high frequency exercise could be proposed to restore hippocampus mitochondrial function and prevent diabetes induced cognitive impairment/encephalopathy.

کلیدواژه ها:

diabetic encephalopaty ، cognitive function ، mitochondria ، exercise ، rhodamine 123 ، learning