Mitochondrial H2O2 emission and cellular redox state link excess fat intake to insulin resistance in both rodents and humans.

By E. Anderson, Mary E. Lustig, K. Boyle, Tracey L. Woodlief, D. Kane, Chien‐Te Lin, J. W. Price, Li Kang, P. Rabinovitch, H. Szeto and 4 more. Journal of Clinical Investigation, 2009

1,168 citations recorded by the source corpus.

Subfields: Cell Biology, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/1e49ae15ea90a2bda592f3a4ece5ee0d0dc5ac3e

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Citations in the corpus

Mechanisms of Insulin Action and Insulin Resistance. (2018, background): “Scavenging mitochondrial H2O2, either through pharmacological means or by transgenically expressing catalase in mitochondria (MCAT mice), protects against HFD-induced muscle insulin resistance (22, 338, 747).”
Signal transduction by reactive oxygen species (2011, background): “In these various animal models, pharmacological or genetic strategies that increase mitochondrial antioxidant levels at least partially reverse the observed metabolic defects (Anderson et al., 2009; Hoehn et al., 2009).”
Glutathione Peroxidase-1 in Health and Disease: From Molecular Mechanisms to Therapeutic Opportunities (2011, neutral): “Thus, in high-fat-induced insulin resistance, excess ROS emanating from mitochondria contribute to insulin insensitivity in skeletal muscle, as overexpression of a mitochondrially targeted catalase in skeletal muscle or acute treatments with antioxidants improve insulin-mediated glucose uptake (7).”
Mitochondrial dysfunction: mechanisms and advances in therapy (2024, background): “294 In addition, ROS signals could be secondary to respiratory alterations-induced insulin sensitivity when subjected to DAG accumulation, PKC θ activation, and impaired muscle insulin signaling.”
Obesity, Oxidative Stress, Adipose Tissue Dysfunction, and the Associated Health Risks: Causes and Therapeutic Strategies (2015, background): “Reduction in mitochondrial ROS production by antioxidant treatment or overexpression of catalase or MnSOD has been found to prevent high-fat diet-induced insulin resistance in mice.(117) These findings suggest that elevated mitochondrial ROS production by excessive metabolic flux promotes insulin re”
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).”
Biomarkers of mitochondrial content in skeletal muscle of healthy young human subjects (2012, background): “Studies on isolated mitochondria or permeabilized muscle fibres have shown that acute exercise (Fernström et al. 2004), high fat diet (Anderson et al. 2009), type 2 diabetes (Phielix et al. 2008), chronic obstructive pulmonary disease (Naimi et al. 2011) and obesity (Anderson et al. 2008) may…”
Fructose and Sugar: A Major Mediator of Nonalcoholic Fatty Liver Disease (2018, positive): “One potential explanation is that, like fructose, high-fat diets induce mitochondrial oxidative stress.(133) Nevertheless, mice lacking fructokinase show marked protection from fatty liver and insulin resistance, highlighting the key role of fructose in western diet-induced NAFLD.”
Inflammation, Defective Insulin Signaling, and Mitochondrial Dysfunction as Common Molecular Denominators Connecting Type 2 Diabetes to Alzheimer Disease (2014, background): “Consumption of a high-fat diet causes increased mitochondrial ROS production and oxidative stress in skeletal muscle, leading to the development of peripheral insulin resistance in T2D (129).”
Sugar consumption, metabolic disease and obesity: The state of the controversy (2015, neutral): “It is also possible that other factors such as inflammation and oxidative stress (51), are contributors to, or possibly mediators of, muscle insulin resistance (52).”
Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010, positive): “Such peptides reduce intracellular ROS and cell death in neuronal (256) and pancreatic islet cells (309) and recently were reported to reduce skeletal myocyte H2O2 production and to preserve insulin sensitivity in rats fed a high-fat diet (14).”