A 15-week running exercise program preserved cardiac function, prevented myocardial apoptosis and fibrosis, and improved mitochondrial biogenesis in mice with advanced diabetic cardiomyopathy.
Does a running exercise program prevent cardiac injury and improve mitochondrial biogenesis in seven-week old male C57BL/6 wild-type or db/db mice?
Exercise preserves cardiac function and improves mitochondrial biogenesis in a mouse model of advanced diabetic cardiomyopathy, potentially via PGC-1α and Akt signaling.
BACKGROUND/AIMS: Diabetic cardiomyopathy (DCM) represents the major cause of morbidity and mortality among diabetics. Exercise has been reported to be effective to protect the heart from cardiac injury during the development of DCM. However, the potential cardioprotective effect of exercise in advanced DCM remains unclear. METHODS: Seven-week old male C57BL/6 wild-type or db/db mice were either subjected to a running exercise program for 15 weeks or kept sedentary. Cardiac function, myocardial apoptosis and fibrosis, and mitochondrial biogenesis were examined for evaluation of cardiac injury. RESULTS: A reduction in ejection fraction and fractional shortening in db/db mice was significantly reversed by exercise training. DCM induced remarkable cardiomyocyte apoptosis and increased ratio of Bax/Bcl-2 at the protein level. Meanwhile, DCM caused slightly myocardial fibrosis with elevated mRNA levels of collagen I and collagen III. Also, DCM resulted in a reduction of mitochondrial DNA (mtDNA) replication and transcription, together with reduced mtDNA content and impaired mitochondrial ultrastructure. All of these changes could be abolished by exercise training. Furthermore, DCM-associated inhibition of PGC-1α and Akt signaling was significantly activated by exercise, indicating that exercise-induced activation of PGC-1α and Akt signaling might be responsible for mediating cardioprotective effect of exercise in DCM. CONCLUSION: Exercise preserves cardiac function, prevents myocardial apoptosis and fibrosis, and improves mitochondrial biogenesis in the late stage of DCM. Exercise-induced activation of PGC-1α and Akt signaling might be promising therapeutic targets for advanced DCM.
Wang et al. (Thu,) conducted a other in Advanced Diabetic Cardiomyopathy. Running exercise program vs. Sedentary was evaluated on Cardiac function, myocardial apoptosis and fibrosis, and mitochondrial biogenesis. A 15-week running exercise program preserved cardiac function, prevented myocardial apoptosis and fibrosis, and improved mitochondrial biogenesis in mice with advanced diabetic cardiomyopathy.