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High-Intensity Interval Training Improves Cardiac Function by miR-206 Dependent HSP60 Induction in Diabetic Rats

  • Objective: A role for microRNAs is implicated in several biological and pathological processes. We investigated the effects of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) on molecular markers of diabetic cardiomyopathy in rats. Methods: Eighteen male Wistar rats (260 ± 10 g; aged 8 weeks) with streptozotocin (STZ)-induced type 1 diabetes mellitus (55 mg/kg, IP) were randomly allocated to three groups: control, MICT, and HIIT. The two different training protocols were performed 5 days each week for 5 weeks. Cardiac performance (end-systolic and end-diastolic dimensions, ejection fraction), the expression of miR-206, HSP60, and markers of apoptosis (cleaved PARP and cytochrome C) were determined at the end of the exercise interventions. Results: Both exercise interventions (HIIT and MICT) decreased blood glucose levels and improved cardiac performance, with greater changes in the HIIT group (p < 0.001, η2: 0.909). While the expressions of miR-206 and apoptotic markers decreased in bothObjective: A role for microRNAs is implicated in several biological and pathological processes. We investigated the effects of high-intensity interval training (HIIT) and moderate-intensity continuous training (MICT) on molecular markers of diabetic cardiomyopathy in rats. Methods: Eighteen male Wistar rats (260 ± 10 g; aged 8 weeks) with streptozotocin (STZ)-induced type 1 diabetes mellitus (55 mg/kg, IP) were randomly allocated to three groups: control, MICT, and HIIT. The two different training protocols were performed 5 days each week for 5 weeks. Cardiac performance (end-systolic and end-diastolic dimensions, ejection fraction), the expression of miR-206, HSP60, and markers of apoptosis (cleaved PARP and cytochrome C) were determined at the end of the exercise interventions. Results: Both exercise interventions (HIIT and MICT) decreased blood glucose levels and improved cardiac performance, with greater changes in the HIIT group (p < 0.001, η2: 0.909). While the expressions of miR-206 and apoptotic markers decreased in both training protocols (p < 0.001, η2: 0.967), HIIT caused greater reductions in apoptotic markers and produced a 20% greater reduction in miR-206 compared with the MICT protocol (p < 0.001). Furthermore, both training protocols enhanced the expression of HSP60 (p < 0.001, η2: 0.976), with a nearly 50% greater increase in the HIIT group compared with MICT. Conclusions: Our results indicate that both exercise protocols, HIIT and MICT, have the potential to reduce diabetic cardiomyopathy by modifying the expression of miR-206 and its downstream targets of apoptosis. It seems however that HIIT is even more effective than MICT to modulate these molecular markers.show moreshow less

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Author details:Maryam DelfanORCiD, Raheleh Amadeh JuybariORCiD, Sattar Gorgani-FiruzjaeeORCiD, Jens Høiriis NielsenORCiDGND, Neda DelfanORCiD, Ismail LaherORCiDGND, Ayoub SaeidiORCiD, Urs GranacherORCiDGND, Hassane ZouhalORCiD
URN:urn:nbn:de:kobv:517-opus4-567238
DOI:https://doi.org/10.25932/publishup-56723
ISSN:1866-8364
Title of parent work (German):Zweitveröffentlichungen der Universität Potsdam : Humanwissenschaftliche Reihe
Publication series (Volume number):Zweitveröffentlichungen der Universität Potsdam : Humanwissenschaftliche Reihe (802)
Further contributing person(s):Jian Shi, Dongtak Jeong, Shun Yan, Pingzhu Zhou
Publication type:Postprint
Language:English
Date of first publication:2022/11/17
Publication year:2022
Publishing institution:Universität Potsdam
Release date:2022/11/17
Tag:apoptosis; cardiomyopathy; diabetes; exercise; miRNAs
Issue:802
Number of pages:11
Organizational units:Humanwissenschaftliche Fakultät / Strukturbereich Kognitionswissenschaften
DDC classification:6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit / 610 Medizin und Gesundheit
Peer review:Referiert
Publishing method:Open Access / Green Open-Access
License (German):License LogoCC-BY - Namensnennung 4.0 International
External remark:Bibliographieeintrag der Originalveröffentlichung/Quelle
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