The DOI matches its Crossref record; 88 of the 89 references it cites were found in a registry or an index.
Linking mitochondrial bioenergetics to insulin resistance via redox biology
Open accessAbstract
Chronic overnutrition and physical inactivity are major risk factors for insulin resistance and type 2 diabetes. Recent research indicates that overnutrition generates an increase in hydrogen peroxide (H(2)O(2)) emission from mitochondria, serving as a release valve to relieve the reducing pressure created by fuel overload, as well as a primary signal that ultimately decreases insulin sensitivity. H(2)O(2) is a major input to cellular redox circuits that link to cysteine residues throughout the entire proteome to regulate cell function. Here we review the principles of mitochondrial bioenergetics and redox systems biology and offer new insight into how H(2)O(2) emission may be linked via redox biology to the etiology of insulin resistance.
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“Emergent evidence suggests that a chronic positive energy balance increases by-products of mitochondrial metabolism that may trigger the pathogenesis of insulin resistance and metabolic inflexibility (16,17).”
From Defects in mitochondrial efficiency and H2O2 emissions in obese women are restored to a lean phenotype with aerobic exercise training (2015) · cites this paper as [17]
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“The nutrient burden creates a positive mitochondrial membrane potential, which increases mtH2O2 emissions (17), and chronic exposure to reactive oxygen species has been shown to inhibit insulin-mediated GLUT4 translocation (26).”
From Defects in mitochondrial efficiency and H2O2 emissions in obese women are restored to a lean phenotype with aerobic exercise training (2015) · cites this paper as [17]
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Cites
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Cited by
Sorted by citations
Mechanisms of Insulin Action and Insulin Resistance
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The aetiology and molecular landscape of insulin resistance
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Comprehensive review on lactate metabolism in human health
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“Pyruvate is then reduced to L-lactate by LDH (Glinghammar et al., 2009).”
BackgroundInfluentialDiabetes and the Brain: Oxidative Stress, Inflammation, and Autophagy
Muriach, M., Flores‐Bellver, M., Romero, F. J., & Barcia, J. M. (2014) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2014/102158 · Cited by 495
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BackgroundThe rise of mitochondria in medicine
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“The detrimental effect of metabolic oversupply is thought to result from mitochondrial substrate overload (Fisher-Wellman and Neufer, 2012), which entails excessive reduction of the respiratory chain and consequent ROS production (Anderson et al., 2009), mitochondrial fission and oxidative stress…”
Background
Metadata
- Authors
- Fisher-Wellman, K. H., & Neufer, P. D.
- Affiliations
- East Carolina University (US)
- Corresponding author
- Neufer, P. Darrell
- ORCID
- Neufer, P. Darrell
- Venue
- Trends in Endocrinology & Metabolism
- Publisher
- Elsevier BV
- Published
- 2012-03
- Volume
- 23
- Issue
- 3
- Pages
- 142-153
- ISSN
- 1043-2760 (ISSN-L)
- PMC
- PMC3313496
- OpenAlex
- W2069466682
- Cited by
- 316
- References
- 89
- Citations by year
- 2026: 17 · 2025: 12 · 2024: 16 · 2023: 22 · 2022: 14 · 2021: 24 · 2020: 16 · 2019: 28 · 2018: 24 · 2017: 25 · 2016: 20 · 2015: 25 · 2014: 29 · 2013: 30 · 2012: 12
- FWCI
- 2.80
- Type
- journal article
- Language
- en
- Open access
- green
- europepmc.org
- Locations
- Trends in Endocrinology and Metabolism (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK073488, R01DK074825)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Keywords
- mitochondrial bioenergetics, insulin resistance, type 2 diabetes, hydrogen peroxide, mitochondrial reactive oxygen species, redox signaling, cysteine residues, overnutrition, physical inactivity
- MeSH terms
- Animals, Energy Metabolism, Humans, Hydrogen Peroxide, Insulin Resistance, Mitochondria, Oxidation-Reduction, Signal Transduction
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