The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
Reduced Mitochondrial Oxidative Capacity and Increased Mitochondrial Uncoupling Impair Myocardial Energetics in Obesity
Abstract
Background— Obesity is a risk factor for cardiovascular disease and is strongly associated with insulin resistance and type 2 diabetes. Recent studies in obese humans and animals demonstrated increased myocardial oxygen consumption (MV̇ o 2 ) and reduced cardiac efficiency (CE); however, the underlying mechanisms remain unclear. The present study was performed to determine whether mitochondrial dysfunction and uncoupling are responsible for reduced cardiac performance and efficiency in ob/ob mice. Methods and Results— Cardiac function, MV̇ o 2 , mitochondrial respiration, and ATP synthesis were measured in 9-week-old ob/ob and control mouse hearts. Contractile function and MV̇ o 2 in glucose-perfused ob/ob hearts were similar to controls under basal conditions but were reduced under high workload. Perfusion of ob/ob hearts with glucose and palmitate increased MV̇ o 2 and reduced CE by 23% under basal conditions, and CE remained impaired at high workload. In glucose-perfused ob/ob hearts, mitochondrial state 3 respirations were reduced but ATP/O ratios were unchanged. In contrast, state 3 respiration rates were similar in ob/ob and control mitochondria from hearts perfused with palmitate and glucose, but ATP synthesis rates and ATP/O ratios were significantly reduced in ob/ob , which suggests increased mitochondrial uncoupling. Pyruvate dehydrogenase activity and protein levels of complexes I, III, and V were reduced in obese mice. Conclusions— These data indicate that reduced mitochondrial oxidative capacity may contribute to cardiac dysfunction in ob/ob mice. Moreover, fatty acid but not glucose-induced mitochondrial uncoupling reduces CE in obese mice by limiting ATP production and increasing MV̇ o 2 .
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“For example, while some groups have reported cardiac hypertrophy in hearts of young ob/ob mice (30, 34, 227), others have only observed this phenotype in older animals (23, 24).”
From Cardiac remodeling in obesity (2008) · cites this paper as [30]
In the citing paper
“In isovolumic ob/ob hearts, although cardiac performance was similar at low work loads, there was a significant reduction at increased work loads (30).”
From Cardiac remodeling in obesity (2008) · cites this paper as [30]
Citations
Cites
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Superoxide activates mitochondrial uncoupling proteins
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Abnormal Cardiac and Skeletal Muscle Energy Metabolism in Patients With Type 2 Diabetes
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Cited by
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Myocardial Fatty Acid Metabolism in Health and Disease
Lopaschuk, G. D., Ussher, J. R., Folmes, C. D. L., Jaswal, J. S., & Stanley, W. C. (2010) · Physiological Reviews · doi:10.1152/physrev.00015.2009 · Cited by 2,228
Cardiac Energy Metabolism in Heart Failure
Lopaschuk, G. D., Karwi, Q. G., Tian, R., Wende, A. R., & Abel, E. D. (2021) · Circulation Research · doi:10.1161/circresaha.121.318241 · Cited by 1,458
Self-citationDiabetic Cardiomyopathy Revisited
Boudina, S., & Abel, E. D. (2007) · Circulation · doi:10.1161/circulationaha.106.679597 · Cited by 1,543
Self-citationRole of Mitochondrial Dysfunction in Insulin Resistance
Kim, J.-A., Wei, Y., & Sowers, J. R. (2008) · Circulation Research · doi:10.1161/circresaha.107.165472 · Cited by 1,103
Molecular mechanisms of diabetic cardiomyopathy
Bugger, H., & Abel, E. D. (2014) · Diabetologia · doi:10.1007/s00125-014-3171-6 · Cited by 903
“ATP synthesis from oxygen consumption, leading to energy depletion [75, 76].”
Self-citation
Metadata
- Authors
- Boudina, S., Sena, S., O’Neill, B. T., Tathireddy, P., Young, M. E., & Abel, E. D.
- Affiliations
- Baylor College of Medicine (US)
- From the Division of Endocrinology, Metabolism and Diabetes and Program in Human Molecular Biology and Genetics (S.B., S.S., B.T.O., P.T., E.D.A.), University of Utah School of Medicine, Salt Lake City, Utah, and USDA/ARS Children’s Nutrition Research Center and Department of Pediatrics (M.E.Y.), Baylor College of Medicine, Houston, Tex.
- Venue
- Circulation
- Published
- 2005-10-25
- Volume
- 112
- Issue
- 17
- Pages
- 2686-2695
- ISSN
- 0009-7322 (ISSN-L)
- 1524-4539
- OpenAlex
- W2160331251
- Cited by
- 502
- References
- 31
- Citations by year
- 2026: 7 · 2025: 12 · 2024: 20 · 2023: 17 · 2022: 22 · 2021: 23 · 2020: 23 · 2019: 16 · 2018: 20 · 2017: 29 · 2016: 25 · 2015: 42 · 2014: 48 · 2013: 39 · 2012: 33
- FWCI
- 6.15
- Type
- journal article
- Language
- en
- Update notices
- correction (2021-12-06)
- Open access
- closed
- Locations
- Circulation (publishedVersion)
- PubMed (publishedVersion)
- Funders
- American Diabetes Association
- American Heart Association
- National Institutes of Health
- National Heart, Lung, and Blood Institute (R01HL073167, R01-HL-73167, UO1HL70525, U01HL070525)
- National Institute of Diabetes and Digestive and Kidney Diseases (R01DK092065)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiovascular Function and Risk Factors
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
- Keywords
- obesity, mitochondrial uncoupling, mitochondrial oxidative capacity, myocardial oxygen consumption, cardiac efficiency, cardiac energetics, ob/ob mice, palmitate, fatty acid metabolism, pyruvate dehydrogenase, mitochondrial respiration, ATP production, insulin resistance, type 2 diabetes, cardiac contractile function
- MeSH terms
- Adenosine Triphosphate, Animals, Energy Metabolism, Mice, Inbred C57BL, Mice, Obese, Mitochondria, Heart, Myocardium, Obesity, Oxidative Phosphorylation, Oxygen Consumption, Mice
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