Ventricular remodeling in growing rats with experimental diabetes: The impact of swimming training

Silva, Edson; Natali, Antônio José; Silva, Márcia F.; Gomes, Gilton J.; Cunha, Daise Nunes Queiroz da; Ramos, Regiane Maria Soares; Toledo, Marileila Marques; Drummond, Filipe Rios; Belfort, Felipe G.; Novaes, Rômulo Dias; Maldonado, Izabel R.S.C.

doi:10.1016/j.prp.2013.06.009

Cited by 17 publications

(9 citation statements)

References 53 publications

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“…In the present study, we observed that diabetes led to increased TGF-β1 mRNA and protein, while the exercise protocol changed the tendency and male reduction of TGF-β1 mRNA and protein. Consistent with previous finding on diabetic rats, 8 weeks' swimming training ameliorated the quantity of collagen in the left ventricle [7]. suggesting that exercise was able to reverse the adverse effect of TGF-β1 on myocardium of diabetic mice, it is probably the mechanism that exercise ameliorates myocardial fibrosis in diabetes.…”

Section: Discussionsupporting

confidence: 90%

The Role and Mechanism of Exercise for Prevention of Myocardial Fibrosis in Diabetes

Zhu¹

2018

Proceedings of the 2018 International Workshop on Bioinformatics, Biochemistry, Biomedical Sciences (BBBS 2018)

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Abstract. Aims. TGF-β1 plays a role in promoting the transformation of myocardial fibrosis. Smad4 has important functions in maintaining tissue stability and inhibiting cardiac hypertrophy. In this study, we investigated the effect of exercise on TGF-β1/Smad4 and myocardial fibrosis in diabetes. Methods. Male C57BL/6 and db/db mice in exercise group were conducted swimming training for 10 weeks. Mice in control group were sedentary. After exercise intervention, heart weight, body weight and blood glucose were observed. TGF-β1, Smad4 and MMP9 in Cardiac tissues were tested through Western blot. The mRNA lever of TGF-β1 and Smad4 were tested through qRT-PCR. Results. Compared to db/db sedentary group, blood glucose in db/db exercise group reduced significantly (P ＜0.05), Heart Index was higher in db/db exercise group than that of db/db sedentary group (P＜0.05). 10 weeks' swimming training reduced the level of TGF-β1 mRNA, protein and Smad4, MMP9 protein in db/db mice significantly (P＜0.05). Conclusion. Aerobic exercise can improve myocardial fibrosis in diabetes through TGF-β1/Smad4 pathway.

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Section: Discussionsupporting

confidence: 90%

The Role and Mechanism of Exercise for Prevention of Myocardial Fibrosis in Diabetes

Zhu¹

2018

Proceedings of the 2018 International Workshop on Bioinformatics, Biochemistry, Biomedical Sciences (BBBS 2018)

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“…From a physiological point of view, beneficial cardiovascular effects following aquatic/swimming training were reported in the animal model. A swimming training program of 90 min per day, 5 days a week performed for 8 weeks proved to be effective in attenuating myocardial fibrosis and contractile dysfunction [148], reduced cardiac glycogen storage [149] and level of tumor necrosis factor-α (TNF-α), and increased capillary density [150] in Wistar rats with streptozotocin-induced DM. Overall, in these rats without antidiabetic drug therapy, an 8-week swimming workout was able to mitigate the vast majority of the pathological changes related to DM.…”

Section: Exercise As Therapy For Diabetes Mellitus: Unconventional Anmentioning

confidence: 99%

Diabetic Cardiomyopathy and Ischemic Heart Disease: Prevention and Therapy by Exercise and Conditioning

Crisafulli

Pagliaro

Roberto

et al. 2020

IJMS

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Metabolic syndrome, diabetes, and ischemic heart disease are among the leading causes of death and disability in Western countries. Diabetic cardiomyopathy is responsible for the most severe signs and symptoms. An important strategy for reducing the incidence of cardiovascular disease is regular exercise. Remote ischemic conditioning has some similarity with exercise and can be induced by short periods of ischemia and reperfusion of a limb, and it can be performed in people who cannot exercise. There is abundant evidence that exercise is beneficial in diabetes and ischemic heart disease, but there is a need to elucidate the specific cardiovascular effects of emerging and unconventional forms of exercise in people with diabetes. In addition, remote ischemic conditioning may be considered among the options to induce beneficial effects in these patients. The characteristics and interactions of diabetes and ischemic heart disease, and the known effects of exercise and remote ischemic conditioning in the presence of metabolic syndrome and diabetes, are analyzed in this brief review.

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“…The benefit of exercise on the prevention and treatment of diabetes and its associated cardiac dysfunction has increasingly been reported [12][13][14][15]. It has been shown in animal models that exercise could prevent ventricular remodeling, attenuate derangement of glucose and lipid metabolism, and improve mitochondrial function and antioxidant capacity, thus leading to ameliorated cardiac performance in the early stage of DCM [16][17][18][19][20][21][22][23]. However, little is known about the effect of exercise on the late stage of DCM at an advanced age.…”

Section: Introductionmentioning

confidence: 99%

Exercise Prevents Cardiac Injury and Improves Mitochondrial Biogenesis in Advanced Diabetic Cardiomyopathy with PGC-1α and Akt Activation

Wang

Bei

et al. 2015

Cell Physiol Biochem

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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 fbrosis, 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.

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Ventricular remodeling in growing rats with experimental diabetes: The impact of swimming training

Cited by 17 publications

References 53 publications

The Role and Mechanism of Exercise for Prevention of Myocardial Fibrosis in Diabetes

The Role and Mechanism of Exercise for Prevention of Myocardial Fibrosis in Diabetes

Diabetic Cardiomyopathy and Ischemic Heart Disease: Prevention and Therapy by Exercise and Conditioning

Exercise Prevents Cardiac Injury and Improves Mitochondrial Biogenesis in Advanced Diabetic Cardiomyopathy with PGC-1α and Akt Activation

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