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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]
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“However, similar PGC1adriven processes in other insulin-resistant models such as the obesity animal model (ob/ob) were not evident [105].”
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“The common way of assessing efficiency in ex vivo rodent hearts is to relate external work (i.e. stroke work, cardiac output, cardiac power, rate pressure product) to MVO2 (Sarnhoff et al. 1958, Mazumder et al. 2004, Boudina et al. 2005, Buchanan et al. 2005, Wang et al. 2005a).”
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Dysregulation of the Mitochondrial Proteome Occurs in Mice Lacking Adiponectin Receptor 1
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“The HFD-feeding associated downregulation of AdipoR1 detected in heart, kidneys and liver suggests that impaired gene expression of OXPHOS proteins in diabetic complications may, at least in part, be driven by impaired AdipoR1/adiponectin signaling, in particular in diabetic cardiomyopathy (37, 38).”
BackgroundMitofilin: Key factor in diabetic cardiomyopathy?
Gorr, M. W., & Wold, L. E. (2014) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2014.11.028 · Cited by 9
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“Studies in rats and humans have shown that obesity is associated with changes in mitochondrial size and density, affecting the activity of the electron transport chain and the capacity for fatty acid oxidation [24, 25].”
Mitochondrial Coupling and Contractile Efficiency in Humans with High and Low V˙O2peaks
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“Changes between minute 3 and the last point of the exercise ($pH(3)) were not significantly different between groups (Mann–Whitney U: P 9 0.”
BackgroundMitochondria and Heart Disease
Stoll, S., Leimena, C., & Qiu, H. (2018) · InTech eBooks · doi:10.5772/intechopen.72611 · Cited by 8
“Mouse models of type 2 diabetes (db/db and ob/ob) showed dysfunctional mitochondrial state 3 respiration and decline in ATP production [125, 126].”
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Left Ventricular Dysfunction in Human Immunodeficiency Virus Infection
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Diet-induced obesity obstructs insulin signaling in the heart
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High-resolution respirometry with multiple substrates titration in permeabilized myocardial fibers.
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Correction: Cardio-Metabolic Effects of HIV Protease Inhibitors (Lopinavir/Ritonavir)
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The role of acetylation in obesity-induced cardiac metabolic alterations
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Obesity and cardiac function – the role of caloric excess and its reversal
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Assessing the Efficiency of the Diabetic Heart at Subcellular, Tissue and Organ Level
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“Those that are known result from proton conductance directly through the inner membrane, through Uncoupling Proteins (UCPs) [46,47], and the adenine nucleotide transporter (ANT, Figure 1).”
BackgroundInfluentialAlterations in Cardiac Metabolism in Heart Failure
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“…2014) or an unchanged P/O ratio in db / db and ob / ob mice (Boudina et al., 2005, 2007) or Type 2 diabetic rats (Pham et al., 2025) when supported with glucose-derived substrates, but the P/O ratio appeared lower when supplied with glucose plus fatty acid substrates (Boudina et al., 2005, 2007).”
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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