ArticlePhysiological reports2016
Exercise-induced alterations in pancreatic oxidative stress and mitochondrial function in type 2 diabetic Goto-Kakizaki rats.
Article in Physiological reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Molecular, Physical, and Technical Performance Response After a Competitive Match in Male Professional Soccer Players.Antioxidants (Basel, Switzerland) · 2025Article
- Type 2 Diabetes Induces a Pro-Oxidative Environment in Rat Epididymis by Disrupting SIRT1/PGC-1α/SIRT3 Pathway.International journal of molecular sciences · 2022Article
- Alterations in Energy Metabolism, Mitochondrial Function and Redox Homeostasis in GK Diabetic Rat Tissues Treated with Aspirin.Life (Basel, Switzerland) · 2022Article
- Exercise alleviates diabetic complications by inhibiting oxidative stress-mediated signaling cascade and mitochondrial metabolic stress in GK diabetic rat tissues.Frontiers in physiology · 2022Article
- Reviewing physical exercise in non-obese diabetic Goto-Kakizaki rats.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2022Review
- Article
- Effect of Aspirin on Mitochondrial Dysfunction and Stress in the Pancreas and Heart of Goto-Kakizaki Diabetic Rats.Life (Basel, Switzerland) · 2021Article
- Augmentation of Glucotoxicity, Oxidative Stress, Apoptosis and Mitochondrial Dysfunction in HepG2 Cells by Palmitic Acid.Nutrients · 2019Article
- Impact of chronic exercise on counteracting chronic stress-induced functional and morphological pancreatic changes in male albino rats.Cell stress & chaperones · 2019Article
- Elucidation of Molecular Mechanisms of Streptozotocin-Induced Oxidative Stress, Apoptosis, and Mitochondrial Dysfunction in Rin-5F PancreaticOxidative medicine and cellular longevity · 2017Article
- Exercise-induced alterations in pancreatic oxidative stress and mitochondrial function in type 2 diabetic Goto-Kakizaki rats.Physiological reports · 2016Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progressive metabolic complications accompanied by oxidative stress are the hallmarks of type 2 diabetes. The precise molecular mechanisms of the disease complications, however, remain elusive. Exercise-induced nontherapeutic management of type 2 diabetes is the first line of choice to control hyperglycemia and diabetes associated complications. In this study, using 11-month-old type 2 Goto-Kakizaki (GK) rats, we have investigated the effects of exercise on mitochondrial metabolic and oxidative stress in the pancreas. Our results showed an increase in theNADPHoxidase enzyme activity and reactive oxygen species (ROS) production inGKrats, which was inhibited after exercise. Increased lipid peroxidation and protein carbonylation andSODactivity were also inhibited after exercise. Interestingly, glutathione (GSH) level was markedly high in the pancreas ofGKdiabetic rats even after exercise. However,GSH-peroxidase andGSH-reductase activities were significantly reduced. Exercise also induced energy metabolism as observed by increased hexokinase and glutamate dehydrogenase activities. A significant decrease in the activities of mitochondrial ComplexesII/IIIandIVwere observed in theGKrats. Exercise improved only ComplexIVactivity suggesting increased utilization of oxygen. We also observed increased activities of cytochrome P450s in the pancreas ofGKrats which was reduced significantly after exercise.SDS-PAGEresults have shown a decreased expression ofNF-κB, Glut-2, andPPAR-ϒ inGKrats which was markedly increased after exercise. These results suggest differential oxidative stress and antioxidant defense responses after exercise. Our results also suggest improved mitochondrial function and energy utilization in the pancreas of exercisingGKrats.
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