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Article: Exercise enhances cardiac function by improving mitochondrial dysfunction and maintaining energy homoeostasis in the development of diabetic cardiomyopathy

TitleExercise enhances cardiac function by improving mitochondrial dysfunction and maintaining energy homoeostasis in the development of diabetic cardiomyopathy
Authors
KeywordsDiabetic cardiomyopathy
Exercise
Mitochondrial dysfunction
Energy metabolism
PGC-1α
Issue Date2020
PublisherSpringer. The Journal's web site is located at http://www.springer.com/biomed/molecular/journal/109
Citation
Journal of Molecular Medicine, 2020, v. 98 n. 2, p. 245-261 How to Cite?
AbstractDiabetic cardiomyopathy (DCM) is a major cause of morbidity and mortality in diabetic patients. Reactive oxygen species (ROS) produced by oxidative stress play an important role in the development of DCM. DCM involves abnormal energy metabolism, thereby reducing energy production. Exercise has been reported to be effective in protecting the heart against ROS accumulation during the development of DCM. We hypothesize that the AMPK/PGC-1α axis may play a crucial role in exercise-induced bioenergetic metabolism and aerobic respiration on oxidative stress parameters in the development of diabetic cardiomyopathy. Using a streptozotocin/high-fat diet mouse to generate a diabetic model, our aim was to evaluate the effects of exercise on the cardiac function, mitochondrial oxidative capacity, mitochondrial function, and cardiac expression of PGC-1α. Mice fed a high-fat diet were given MO-siPGC-1α or treated with AMPK inhibitor. Mitochondrial structure and effects of switching between the Warburg effect and aerobic respiration were analysed. Exercise improved blood pressure and systolic dysfunction in diabetic mouse hearts. The beneficial effects of exercise were also observed in a mitochondrial function study, as reflected by an enhanced oxidative phosphorylation level, increased membrane potential, and decreased ROS level and oxygen consumption. On the other hand, depletion of PGC-1α attenuated the effects of exercise on the enhancement of mitochondrial function. In addition, PGC-1α may be responsible for reversing the Warburg effect to aerobic respiration, thus enhancing mitochondrial metabolism and energy homoeostasis. In this study, we demonstrate the protective effects of exercise on shifting energy metabolism from fatty acid oxidation to glucose oxidation in an established diabetic stage. These data suggest that exercise is effective at ameliorating diabetic cardiomyopathy by improving mitochondrial function and reducing metabolic disturbances.
Persistent Identifierhttp://hdl.handle.net/10722/288410
ISSN
2019 Impact Factor: 4.427
2015 SCImago Journal Rankings: 2.165

 

DC FieldValueLanguage
dc.contributor.authorWANG, SY-
dc.contributor.authorZhu, S-
dc.contributor.authorWu, JIAN-
dc.contributor.authorZhang, M-
dc.contributor.authorXu, Y-
dc.contributor.authorXu, W-
dc.contributor.authorCui, J-
dc.contributor.authorYu, B-
dc.contributor.authorCao, W-
dc.contributor.authorLiu, J-
dc.date.accessioned2020-10-05T12:12:29Z-
dc.date.available2020-10-05T12:12:29Z-
dc.date.issued2020-
dc.identifier.citationJournal of Molecular Medicine, 2020, v. 98 n. 2, p. 245-261-
dc.identifier.issn0946-2716-
dc.identifier.urihttp://hdl.handle.net/10722/288410-
dc.description.abstractDiabetic cardiomyopathy (DCM) is a major cause of morbidity and mortality in diabetic patients. Reactive oxygen species (ROS) produced by oxidative stress play an important role in the development of DCM. DCM involves abnormal energy metabolism, thereby reducing energy production. Exercise has been reported to be effective in protecting the heart against ROS accumulation during the development of DCM. We hypothesize that the AMPK/PGC-1α axis may play a crucial role in exercise-induced bioenergetic metabolism and aerobic respiration on oxidative stress parameters in the development of diabetic cardiomyopathy. Using a streptozotocin/high-fat diet mouse to generate a diabetic model, our aim was to evaluate the effects of exercise on the cardiac function, mitochondrial oxidative capacity, mitochondrial function, and cardiac expression of PGC-1α. Mice fed a high-fat diet were given MO-siPGC-1α or treated with AMPK inhibitor. Mitochondrial structure and effects of switching between the Warburg effect and aerobic respiration were analysed. Exercise improved blood pressure and systolic dysfunction in diabetic mouse hearts. The beneficial effects of exercise were also observed in a mitochondrial function study, as reflected by an enhanced oxidative phosphorylation level, increased membrane potential, and decreased ROS level and oxygen consumption. On the other hand, depletion of PGC-1α attenuated the effects of exercise on the enhancement of mitochondrial function. In addition, PGC-1α may be responsible for reversing the Warburg effect to aerobic respiration, thus enhancing mitochondrial metabolism and energy homoeostasis. In this study, we demonstrate the protective effects of exercise on shifting energy metabolism from fatty acid oxidation to glucose oxidation in an established diabetic stage. These data suggest that exercise is effective at ameliorating diabetic cardiomyopathy by improving mitochondrial function and reducing metabolic disturbances.-
dc.languageeng-
dc.publisherSpringer. The Journal's web site is located at http://www.springer.com/biomed/molecular/journal/109-
dc.relation.ispartofJournal of Molecular Medicine-
dc.rightsThis is a post-peer-review, pre-copyedit version of an article published in [insert journal title]. The final authenticated version is available online at: https://doi.org/[insert DOI]-
dc.subjectDiabetic cardiomyopathy-
dc.subjectExercise-
dc.subjectMitochondrial dysfunction-
dc.subjectEnergy metabolism-
dc.subjectPGC-1α-
dc.titleExercise enhances cardiac function by improving mitochondrial dysfunction and maintaining energy homoeostasis in the development of diabetic cardiomyopathy-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1007/s00109-019-01861-2-
dc.identifier.pmid31897508-
dc.identifier.scopuseid_2-s2.0-85077587652-
dc.identifier.hkuros315781-
dc.identifier.volume98-
dc.identifier.issue2-
dc.identifier.spage245-
dc.identifier.epage261-
dc.publisher.placeGermany-

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