ArticleMolecular and cellular biochemistry2018
The role of mitochondrial DNA damage at skeletal muscle oxidative stress on the development of type 2 diabetes.
Article in Molecular and cellular biochemistry, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 49 citations in OpenAlex.
- Ubiquitin-Specific Protease 2 (USP2) as a Modulator of Energy Metabolism: A Review of Studies Using Animal and Cellular Models.Biomedicines · 2026Review
- The Integration of Bioinformatics with Experimental Validation Has Uncovered Shared Molecular Characteristics Between Sarcopenia and Osteoarthritis.Calcified tissue international · 2026Article
- The Perfect Cup? Coffee-Derived Polyphenols and Their Roles in Mitigating Factors Affecting Type 2 Diabetes Pathogenesis.Molecules (Basel, Switzerland) · 2024Review
- Mitochondrial Dysfunction, Oxidative Stress, and Inter-Organ Miscommunications in T2D Progression.International journal of molecular sciences · 2024Review
- Novel targets and therapies of metformin in dementia: old drug, new insights.Frontiers in pharmacology · 2024Review
- Determination and characterization of molecular heterogeneity and precision medicine strategies of patients with pancreatic cancer and pancreatic neuroendocrine tumor based on oxidative stress and mitochondrial dysfunction-related genes.Frontiers in endocrinology · 2023Article
- Knockdown of mitochondrial threonyl-tRNA synthetase 2 inhibits lung adenocarcinoma cell proliferation and induces apoptosis.Bioengineered · 2022Article
- A higher mitochondrial content is associated with greater oxidative damage, oxidative defenses, protein synthesis and ATP turnover in resting skeletal muscle.The Journal of experimental biology · 2021Article
- Sphingolipids as a Culprit of Mitochondrial Dysfunction in Insulin Resistance and Type 2 Diabetes.Frontiers in endocrinology · 2021Review
- Transcription of mtDNA and dyslipidemia are ameliorated by aerobic exercise in type 2 diabetes.Molecular biology reports · 2020Article
- Improvement of skeletal muscle insulin sensitivity by 1 week of SGLT2 inhibitor use.Endocrine connections · 2020Article
- Potential Protective Effect of Dietary Intake of Non-Oxidative medicine and cellular longevity · 2020Article
- Skimmin Improves Insulin ResistanceFrontiers in pharmacology · 2020Article
- Leukocyte Telomere Length Independently Predicts 3-Year Diabetes Risk in a Longitudinal Study of Chinese Population.Oxidative medicine and cellular longevity · 2020Article
- The Role of Oxidative Stress in the Development of Diabetes Mellitus and Its Complications.Journal of diabetes research · 2019Article
- Plasma mitochondrial DNA is elevated in obese type 2 diabetes mellitus patients and correlates positively with insulin resistance.PloS one · 2019Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Reduced cellular response to insulin in skeletal muscle is one of the major components of the development of type 2 diabetes (T2D). Mitochondrial dysfunction involves in the accumulation of toxic reactive oxygen species (ROS) that leads to insulin resistance. The aim of this study was to verify the involvement of mitochondrial DNA damage at ROS generation in skeletal muscle during development of T2D. Wistar rats were fed a diet containing 60% fat over 8 weeks and at day 14 a single injection of STZ (25 mg/kg) was administered (T2D-induced). Control rats received standard food and an injection of citrate buffer. Blood and soleus muscle were collected. Abdominal fat was quantified as well as glucose, triglyceride, LDL, HDL, and total cholesterol in plasma and mtDNA copy number, cytochrome b (cytb) mRNA, 8-hydroxyguanosine, and 8-isoprostane (a marker of ROS) in soleus muscle. T2D-induced animal presented similar characteristics to humans that develop T2D such as changes in blood glucose, abdominal fat, LDL, HDL and cholesterol total. In soleus muscle 8-isoprostane, mtDNA copy number and 8-hydroxyguanosine were increased, while cytb mRNA was decreased in T2D. Our results suggest that in the development of T2D, when risks factors of T2D are present, intracellular oxidative stress increases in skeletal muscle and is associated with a decrease in cytb transcription. To overcome this process mtDNA increased but due to the proximity of ROS generation, mtDNA remains damaged by oxidation leading to an increase in ROS in a vicious cycle accounting to the development of insulin resistance and further T2D.
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