Oxidative stress and the etiology of insulin resistance and type 2 diabetes
Open accessAbstract
The condition of oxidative stress arises when oxidant production exceeds antioxidant activity in cells and plasma. The overabundance of oxidants is mechanistically connected to the multifactorial etiology of insulin resistance, primarily in skeletal muscle tissue, and the subsequent development of type 2 diabetes. Two important mechanisms for this oxidant excess are (1) the mitochondrial overproduction of hydrogen peroxide and superoxide ion under conditions of energy surplus and (2) the enhanced activation of cellular NADPH oxidase via angiotensin II receptors. Several recent studies are reviewed that support the concept that direct exposure of mammalian skeletal muscle to an oxidant stress (including hydrogen peroxide) results in stimulation of the serine kinase p38 mitogen-activated protein kinase (p38 MAPK), and that the engagement of this stress-activated p38 MAPK signaling is mechanistically associated with diminished insulin-dependent stimulation of insulin signaling elements and glucose transport activity. The beneficial interactions between the antioxidant α-lipoic acid and the advanced glycation end-product inhibitor pyridoxamine that ameliorate oxidant stress-associated defects in whole-body and skeletal-muscle insulin action in the obese Zucker rat, a model of prediabetes, are also addressed. Overall, this review highlights the importance of oxidative stress in the development of insulin resistance in mammalian skeletal muscle tissue, at least in part via a p38-MAPK-dependent mechanism, and indicates that interventions that reduce this oxidative stress and oxidative damage can improve insulin action in insulin-resistant animal models. Strategies to prevent and ameliorate oxidative stress remain important in the overall treatment of insulin resistance and type 2 diabetes.
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During a pathophysiological state, a large and sustained increase in ROS impairs insulin action, through the activation of stress signaling pathways (i.e., MAPK and JNK), contributing to the pathogenesis of diet-induced insulin resistance.
“On the other hand, during a pathophysiological state, abundant evidence indicates that a large and sustained increase in ROS impairs insulin action, through the activation of stress signaling pathways (*i.e.,* MAPK and JNK) ([85](#B85), [154](#B154)), contributing to the pathogenesis of diet-induced insulin resistance ([67](#B67)).”
From Mitochondrial fatty acid oxidation in obesity (2013) · cites this paper as [67]
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Self-citation
- Authors
- Henriksen, E. J., Diamond-Stanic, M. K., & Marchionne, E. M.
- Affiliations
- University of Arizona (US)
- Corresponding author
- Henriksen, Erik J.
- Venue
- Free Radical Biology and Medicine
- Publisher
- Elsevier BV
- Published
- 2011-09
- Volume
- 51
- Issue
- 5
- Pages
- 993-999
- ISSN
- 0891-5849 (ISSN-L)
- PMC
- PMC3071882
- OpenAlex
- W2023754969
- Cited by
- 600
- References
- 99
- Citations by year
- 2026: 14 · 2025: 31 · 2024: 42 · 2023: 50 · 2022: 37 · 2021: 43 · 2020: 39 · 2019: 48 · 2018: 52 · 2017: 42 · 2016: 42 · 2015: 41 · 2014: 33 · 2013: 37 · 2012: 41
- FWCI
- 2.39
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Free Radical Biology and Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Heart, Lung, and Blood Institute (T32-HL-07249, T32HL007249)
- National Institute of Diabetes and Digestive and Kidney Diseases (DK-063967, R01DK063967)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Health Sciences › Medicine › Physiology › Nitric Oxide and Endothelin Effects
- Keywords
- oxidative stress, insulin resistance, type 2 diabetes, skeletal muscle, hydrogen peroxide, superoxide, NADPH oxidase, angiotensin II receptor, p38 MAPK, serine kinase, insulin signaling, glucose transport, alpha-lipoic acid, pyridoxamine, advanced glycation end products, prediabetes, Zucker fatty rats
- MeSH terms
- Animals, Antioxidants, Diabetes Mellitus, Type 2, Disease Models, Animal, Energy Metabolism, Humans, Hydrogen Peroxide, Insulin Resistance, Superoxides, Signal Transduction, Reactive Oxygen Species, Oxidative Stress, Muscle, Skeletal, NADPH Oxidases, p38 Mitogen-Activated Protein Kinases
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
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