Document Type : Original Article
Authors
1
Department of Physical Education and Sports Sciences, Faculty of Humanities and Social Sciences, University of Kurdistan, Sanandaj, Kurdistan, Iran.
2
Associate Professor of Exercise Physiology, Department of Exercise Physiology, Faculty of Humanities and Social Sciences, University of Kurdistan, Sanandaj, Iran.
3
Ph D student in exercise physiology, Department of Kinesiology and Sport Management, Texas A&M University, USA.
4
Master’s student of Science in Exercise Physiology, Department of Exercise Physiology, Faculty of Humanities and Social Sciences, University of Kurdistan, Sanandaj, Iran.
Abstract
Introduction: Type 2 diabetes is a common metabolic disorder characterized by elevated blood glucose levels and impaired mitochondrial function. Reduced mitochondrial efficiency in this disease leads to a decline in the mitophagy process, which in turn contributes to the progression of diabetes complications, including insulin resistance and metabolic disorders. Mitophagy, which involves the degradation and recycling of damaged mitochondria, is essential for maintaining cellular health. Parkin, PTEN-induced kinase 1 (PINK-1), and Optineurin (OPTN) are among the key markers of this process. Therefore, identifying strategies to enhance mitophagy in type 2 diabetes may help improve mitochondrial function and mitigate disease complications. One such strategy is exercise, which has been shown to have positive effects on metabolic health and mitochondrial function. This study aimed to investigate the effect of a high-intensity interval training (HIIT) regimen on the content of mitophagy-related proteins, including Parkin, PINK-1, and OPTN, in the visceral adipose tissue of rats with type 2 diabetes.
Methods: In this experimental study, 24 male rats were divided into three groups: healthy control (HC), diabetic control (DC), and diabetic + HIIT exercise (D+HIIT). Type 2 diabetes was induced in the rats through streptozotocin (STZ) injection combined with a high-fat diet (HFD). The exercise group underwent eight weeks of high-intensity interval training (HIIT). The intensity of the HIIT sessions was set at 85–90% of the rats' maximum running speed, while the low-intensity recovery intervals were performed at 50–60% of maximum speed. At the end of the HIIT intervention, visceral adipose tissue was extracted from each group, and the protein content of mitophagy markers, including Parkin, PINK-1, and OPTN, was measured using the Western blot technique.
Results: The results of this study showed that type 2 diabetes led to a significant reduction in the levels of PARKIN (33%), PINK-1 (41%), and OPTN (46%) in the DC group compared to the HC group (p < 0.001). However, in the D+HIIT group, HIIT exercise significantly increased these protein levels compared to the DC group, with PARKIN, PINK-1, and OPTN levels increasing by 117.91%, 103.39%, and 536.36%, respectively (p < 0.001). Additionally, HIIT exercise in the D+HIIT group resulted in a significant reduction in fasting glucose levels and the HOMA-IR index (p < 0.001).
Conclusion: The results of this study indicate that HIIT exercise has significant effects on the restoration of mitophagy-related proteins and the improvement of metabolic indices in visceral adipose tissue in an animal model of type 2 diabetes. These findings highlight the importance of exercise, particularly HIIT, in enhancing mitochondrial function and promoting cellular processes. However, given the animal-based nature of this study, extrapolating the results to patients with type 2 diabetes requires further investigation in human studies.
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