- ObjectiveA 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. MethodsEighteen 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. ResultsBoth exercise interventions (HIIT and MICT) decreased blood glucose levels and improved cardiac performance, with greater changes in the HIIT group (p < 0.001, eta(2): 0.909). While the expressions of miR-206 and apoptotic markers decreased in bothObjectiveA 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. MethodsEighteen 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. ResultsBoth exercise interventions (HIIT and MICT) decreased blood glucose levels and improved cardiac performance, with greater changes in the HIIT group (p < 0.001, eta(2): 0.909). While the expressions of miR-206 and apoptotic markers decreased in both training protocols (p < 0.001, eta(2): 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, eta(2): 0.976), with a nearly 50% greater increase in the HIIT group compared with MICT. ConclusionsOur 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.…
MetadatenAuthor details: | Maryam Delfan, Raheleh Amadeh Juybari, Sattar Gorgani-Firuzjaee, Jens Høiriis Nielsen, Neda Delfan, Ismail Laher, Ayoub Saeidi, Urs GranacherORCiDGND, Hassane Zouhal |
---|
DOI: | https://doi.org/10.3389/fcvm.2022.927956 |
---|
ISSN: | 2297-055X |
---|
Pubmed ID: | https://pubmed.ncbi.nlm.nih.gov/35845054 |
---|
Title of parent work (English): | Frontiers in cardiovascular medicine |
---|
Publisher: | Frontiers Media |
---|
Place of publishing: | Lausanne |
---|
Publication type: | Article |
---|
Language: | English |
---|
Date of first publication: | 2022/06/29 |
---|
Publication year: | 2022 |
---|
Release date: | 2024/06/18 |
---|
Tag: | apoptosis; cardiomyopathy; diabetes; exercise; miRNAs |
---|
Volume: | 9 |
---|
Article number: | 927956 |
---|
Number of pages: | 11 |
---|
Funding institution: | Deutsche Forschungsgemeinschaft (DFG, German Research Foundation); [491466077]; Open Access Publishing Fund of the University of Potsdam,; Germany; Alzahra University |
---|
Organizational units: | Humanwissenschaftliche Fakultät / Strukturbereich Kognitionswissenschaften / Department Sport- und Gesundheitswissenschaften |
---|
DDC classification: | 6 Technik, Medizin, angewandte Wissenschaften / 61 Medizin und Gesundheit |
---|
Peer review: | Referiert |
---|
Publishing method: | Open Access / Gold Open-Access |
---|
| DOAJ gelistet |
---|
License (German): | CC-BY - Namensnennung 4.0 International |
---|