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Increased oxidative stress in obesity and its impact on metabolic syndrome
Open accessAbstract
Obesity is a principal causative factor in the development of metabolic syndrome. Here we report that increased oxidative stress in accumulated fat is an important pathogenic mechanism of obesity-associated metabolic syndrome. Fat accumulation correlated with systemic oxidative stress in humans and mice. Production of ROS increased selectively in adipose tissue of obese mice, accompanied by augmented expression of NADPH oxidase and decreased expression of antioxidative enzymes. In cultured adipocytes, elevated levels of fatty acids increased oxidative stress via NADPH oxidase activation, and oxidative stress caused dysregulated production of adipocytokines (fat-derived hormones), including adiponectin, plasminogen activator inhibitor-1, IL-6, and monocyte chemotactic protein-1. Finally, in obese mice, treatment with NADPH oxidase inhibitor reduced ROS production in adipose tissue, attenuated the dysregulation of adipocytokines, and improved diabetes, hyperlipidemia, and hepatic steatosis. Collectively, our results suggest that increased oxidative stress in accumulated fat is an early instigator of metabolic syndrome and that the redox state in adipose tissue is a potentially useful therapeutic target for obesity-associated metabolic syndrome.
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“Thus, by suppressing adipocyte oxidative stress, spirulina may lead to systemic anti-inflammatory and insulin-sensitising effects.12–20”
From Effects of spirulina on weight loss and blood lipids: A review (2020) · cites this paper as [16]
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“It has been suggested that the production of ROS and RNS by immune cells contribute to the oxidative damage observed in obese AT (74,75).”
From The ominous triad of adipose tissue dysfunction: inflammation, fibrosis, and impaired angiogenesis. (2017) · cites this paper as [74]
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“Obesity is associated with systemic oxidative stress (43, 44), which promotes insulin resistance (11–18).”
From Skeletal muscle NOX4 is required for adaptive responses that prevent insulin resistance (2021) · cites this paper as [43]
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“Increased oxidative stress and reduced antioxidant defense have been demonstrated in obese AT (74).”
From The ominous triad of adipose tissue dysfunction: inflammation, fibrosis, and impaired angiogenesis. (2017) · cites this paper as [74]
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“High levels of ROS and systemic oxidative stress have been associated with obesity and insulin resistance ([45](#B45)).”
From Mitochondrial fatty acid oxidation in obesity (2013) · cites this paper as [45]
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“In addition to inflammation, the AGE-RAGE axis also triggers oxidative stress, which is associated with the development of insulin resistance.[122,123]”
From The Role of Dietary Advanced Glycation End Products in Metabolic Dysfunction (2021) · cites this paper as [122]
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Metadata
- Authors
- Furukawa, S., Fujita, T., Shimabukuro, M., Iwaki, M., Yamada, Y., Nakajima, Y., Nakayama, O., Makishima, M., Matsuda, M., & Shimomura, I.
- Affiliations
- The University of Osaka (JP)
- University of the Ryukyus (JP)
- Nihon University (JP)
- Japan Science and Technology Agency (JP)
- Corresponding author
- Matsuda, Morihiro
- Venue
- Journal of Clinical Investigation
- Published
- 2004-12-15
- Volume
- 114
- Issue
- 12
- Pages
- 1752-1761
- ISSN
- 0021-9738 (ISSN-L)
- PMC
- PMC535065
- OpenAlex
- W2124821727
- Cited by
- 5,508
- References
- 67
- Citations by year
- 2026: 179 · 2025: 219 · 2024: 218 · 2023: 286 · 2022: 289 · 2021: 355 · 2020: 335 · 2019: 365 · 2018: 331 · 2017: 296 · 2016: 316 · 2015: 277 · 2014: 295 · 2013: 295 · 2012: 305
- FWCI
- 79.28
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Clinical Investigation (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Naito Foundation
- Suzuken Memorial Foundation
- Cell Science Research Foundation
- Novartis Foundation
- Japan Research Foundation for Clinical Pharmacology
- Tokyo Biochemical Research Foundation
- Ministry of Education, Culture, Sports, Science and Technology
- Kato Memorial Bioscience Foundation
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- Japan Heart Foundation
- Japan Society for the Promotion of Science
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
- Health Sciences › Medicine › Physiology (medical) › Adipose Tissue and Metabolism
- Keywords
- obesity, metabolic syndrome, oxidative stress, reactive oxygen species, adipose tissue, NADPH oxidase, adipocytes, adipokines, adiponectin, plasminogen activator inhibitor-1, interleukin-6, MCP-1, NADPH oxidase inhibitors, hepatic steatosis, hyperlipidemia, diabetes mellitus, redox state
- MeSH terms
- Adipose Tissue, Aged, Animals, Antioxidants, Body Weight, Cell Differentiation, Dose-Response Relationship, Drug, Female, Humans, Hydrogen Peroxide, Male, Mice, Inbred C57BL, Mice, Obese, Middle Aged, Models, Biological, Obesity, Oxidation-Reduction, RNA, Messenger, Time Factors, Immunoblotting, Lipid Peroxidation, Cytokines, Reactive Oxygen Species, Thiobarbituric Acid Reactive Substances, Adipocytes, Oxidative Stress, NADPH Oxidases, Reverse Transcriptase Polymerase Chain Reaction, Metabolic Syndrome, 3T3-L1 Cells, Mice
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