Role of Mitochondrial Oxidative Stress in Glucose Tolerance, Insulin Resistance, and Cardiac Diastolic Dysfunction
Open accessAbstract
Background: Diabetes mellitus (DM) is associated with mitochondrial oxidative stress. We have shown that myocardial oxidative stress leads to diastolic dysfunction in a hypertensive mouse model. Therefore, we hypothesized that diabetes mellitus could cause diastolic dysfunction through mitochondrial oxidative stress and that a mitochondria‐targeted antioxidant (Mito TEMPO ) could prevent diastolic dysfunction in a diabetic mouse model. Methods and Results: C57 BL /6J mice were fed either 60 kcal % fat diet (high‐fat diet [ HFD ]) or normal chow (control) for 8 weeks with or without concurrent Mito TEMPO administration, followed by in vivo assessment of diastolic function and ex vivo studies. HFD mice developed impaired glucose tolerance compared with the control (serum glucose=495±45 mg/dL versus 236±30 mg/dL at 60 minutes after intraperitoneal glucose injection, P <0.05). Myocardial tagged cardiac magnetic resonance imaging showed significantly reduced diastolic circumferential strain (Ecc) rate in the HFD mice compared with controls (5.0±0.3 1/s versus 7.4±0.5 1/s, P <0.05), indicating diastolic dysfunction in the HFD mice. Systolic function was comparable in both groups (left ventricular ejection fraction=66.4±1.4% versus 66.7±1.2%, P >0.05). Mito TEMPO ‐treated HFD mice showed significant reduction in mitochondria reactive oxygen species, S ‐glutathionylation of cardiac myosin binding protein C, and diastolic dysfunction, comparable to the control. The fasting insulin levels of Mito TEMPO ‐treated HFD mice were also comparable to the controls ( P >0.05). Conclusions: Mito TEMPO treatment prevented insulin resistance and diastolic dysfunction, suggesting that mitochondrial oxidative stress may be involved in the pathophysiology of both conditions.
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Increased formation of ROS in mitochondria is a typical phenomenon in diabetic patients with cardiovascular diseases, typically with left ventricular hypertrophy and diastolic dysfunction.
“Increased formation of ROS in mitochondria is a typical phenomenon in diabetic patients with cardiovascular diseases, typically with left ventricular hypertrophy and diastolic dysfunction (Jeong et al. 2016).”
From Reactive Oxygen Species, Toxicity, Oxidative Stress, and Antioxidants: Chronic Diseases and Aging (2023) · cites this paper as Jeong et al. 2016
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- Authors
- Jeong, E., Chung, J., Liu, H., Go, Y., Gladstein, S., Farzaneh‐Far, A., Lewandowski, E. D., & Dudley, S. C.
- Affiliations
- Brown University (US)
- University of Illinois Chicago (US)
- Rhode Island Hospital (US)
- Corresponding author
- Jeong, Euy‐Myoung
- Chung, Jaehoon
- Dudley, Samuel C.
- ORCID
- Venue
- Journal of the American Heart Association
- Published
- 2016-05-06
- Volume
- 5
- Issue
- 5
- ISSN
- 2047-9980 (ISSN-L)
- PMC
- PMC4889180
- OpenAlex
- W2346053177
- Cited by
- 119
- References
- 36
- Citations by year
- 2026: 8 · 2025: 9 · 2024: 11 · 2023: 17 · 2022: 11 · 2021: 12 · 2020: 11 · 2019: 11 · 2018: 12 · 2017: 15 · 2016: 2
- FWCI
- 11.01
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by-nc
- Locations
- Journal of the American Heart Association (publishedVersion, cc-by-nc)
- PubMed Central (publishedVersion, cc-by-nc)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- National Heart, Lung, and Blood Institute (R01HL049244, R41HL112355, R01HL085520, R01HL106592, R01HL104025, R37HL049244, P01HL058000)
- Topics
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Pathology and Forensic Medicine › Cardiac Ischemia and Reperfusion
- Keywords
- mitochondrial oxidative stress, glucose tolerance, insulin resistance, diastolic dysfunction, MitoTEMPO, mitochondria-targeted antioxidants, high-fat diet, diabetes mellitus, S-glutathionylation, myosin binding protein C, cardiac magnetic resonance imaging, diabetic cardiomyopathy
- MeSH terms
- Animals, Biomechanical Phenomena, Diabetes Mellitus, Experimental, Diabetes Mellitus, Type 2, Diastole, Disease Models, Animal, Glucose, Hemodynamics, Insulin Resistance, Magnetic Resonance Imaging, Mice, Inbred C57BL, Mitochondria, Heart, Cardiomyopathies, Myocardium, Reactive Oxygen Species, Glucose Intolerance, Oxidative Stress, Myocytes, Cardiac, Microscopy, Electron, Transmission, Mice, Heart Failure, Diastolic, Diet, High-Fat
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