Abstract 613: Exercise Training Improves Cardiac Mitofusin 2 Expression In Diabetes

Abstract

Introduction: DM increases the risk of developing cardiovascular disease, although the specific molecular mechanisms underlying DM are not well understood, perhaps the most important pathway regulating metabolism in muscle is mitochondrial biogenesis. The mitofusin 2 is a important protein to mitochondrial fusion. Additionally, muscle mitochondrial metabolism is regulated by a group of morphogenesis machinery proteins which are important for mitochondrial fusion and fission events and also for their independent effects on bioenergetics. The exercise training is a strategy for reversing the effects of mitochondrial dysfunction trough the regulation of mitochondrial protein transcription and biogenegis. The aim of this study was to verify if endurance exercise increases the expression of Mitofusin 2 in cardiac myocytes in experimental diabetes. Male Wistar rats were divided into 4 groups: control (C:8), control trained (CT=8), diabetic (D=8), diabetic trained (DT=8). DM was induced by STZ (50mg/kg). Trained groups were submitted to an exercise training (ET) protocol on a treadmill (8 wk). BPS, HR were analyzed using a data acquisition system (PowerLab). The ratio between heart weight and tibia length was used to determination of cardiac hypertrophy. The expression of protein mitofusin 2 was evaluated by western blotting. The BPS was similar between grups (CS:124, CT:128; DS:122; DT:130 mmHg), however the HR was decreased in the DS group (323bpm) and ET was able to normalize this (DT 342bpm ). DM decreased 23% of the cardiac mass, but ET prevented this reduction (DT 13%). The expression mft2 was reduced in the DS and the exercise normalized this expression. Conclusion: ET was able to avoid the cardiac muscle deterioration leading to the normalization of HR. This hemodynamic adaptation can be related with a bigger expression of mitofusin 2 and it could be associated with an improvement of cardiac metabolism. The importance of ET as a non pharmacological approach to treat the DM complications was demonstrated by the improvement of cardiac function and molecular mechanisms.