Mitochondrial dysfunction results from oxidative stress in the skeletal muscle of diet-induced insulin-resistant mice.
By C. Bonnard, A. Durand, S. Peyrol, E. Chanséaume, M. Chauvin, B. Morio, H. Vidal, J. Rieusset. Journal of Clinical Investigation, 2008
835 citations recorded by the source corpus.
Subfields: Molecular Biology, Physiology
View Paper: https://www.semanticscholar.org/paper/e36eaefa2277791bf761c5fb0ffbf0c22abc1d8c
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
- Orian Shirihai
- M. Palacín
- Matej Oresic
- Sushil Kumar Jain
- R. Burcelin
- Antonio Zorzano
- M. Liesa
- C. Kevil
In Physiology
Citations in the corpus
- Obesity, Oxidative Stress, Adipose Tissue Dysfunction, and the Associated Health Risks: Causes and Therapeutic Strategies (2015, background): “Intake of a highfat diet has been shown to increase mitochondrial ROS production and direct the cellular redox environment to a more oxidized state in skeletal muscle of rodents or humans.(9,117,118) Reduction in mitochondrial ROS production by antioxidant treatment or overexpression of catalase or ”
- Endothelial Dysfunction and Diabetes: Effects on Angiogenesis, Vascular Remodeling, and Wound Healing (2012, background): “Increase of both XO expression and activity results in imbalance of ATP/ADP ratio and increased ROS production in skeletal muscle of STZ-induced diabetic mice [38, 39].”
- Mitochondrial Fission Contributes to Mitochondrial Dysfunction and Insulin Resistance in Skeletal Muscle (2011, background): “Similarly, HF feeding of mice for 4 weeks does not alter their mitochondrial content and respiration rates (3).”
- Mitochondrial Dynamics in the Regulation of Nutrient Utilization and Energy Expenditure (2013, background): “…that increased ROS generation, caused by nutrient excess through long-term feeding of a highsucrose and high-fat diet, is likely to cause self-inflicted oxidative damage to the mitochondria and their dysfunction, the latter taking place after the onset of insulin resistance (Bonnard et al., 2008).”
- Mitofusin 2 (Mfn2) links mitochondrial and endoplasmic reticulum function with insulin signaling and is essential for normal glucose homeostasis (2012, background): “In this regard, a high-fat diet (HFD) causes increased hydrogen peroxide production and oxidative stress in skeletal muscle, which might explain, at least in part, the development of insulin resistance (23, 24).”
- Hyperglycemia and Oxidative Stress: An Integral, Updated and Critical Overview of Their Metabolic Interconnections (2023, background): “In summary, FoxO activation under oxidative stress cannot be enough to be part of the antioxidant response and its inactivation, on the other hand, may increase metabolic disturbances in DMT2 in some tissues.”