Cited by 502Mitochondrial Function and PathologyCardiovascular Function and Risk FactorsCardiac Ischemia and Reperfusion

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Reduced Mitochondrial Oxidative Capacity and Increased Mitochondrial Uncoupling Impair Myocardial Energetics in Obesity

Boudina, Sihem, Sena, Sandra, O’Neill, Brian T., Tathireddy, Prakash, Young, Martin E., Abel, E. Dale·2005·Circulation

DOI 10.1161/circulationaha.105.554360

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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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BackgroundSelf-citation
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Background
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Regulation of fatty acid metabolism by mTOR in adult murine hearts occurs independently of changes in PGC-1α
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“CS activity was assessed in frozen cardiac tissue as previously described (2).”
MethodSelf-citation
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MethodSelf-citation
Cardiac Metabolic Alterations in Hypertensive Obese Pigs
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Background
Retracted
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Background
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“These RCR values are consistent with other publications using heart tissues in ectotherms (2, 21).”
Result
Activation of IGF-1 receptors and Akt signaling by systemic hyperinsulinemia contributes to cardiac hypertrophy but does not regulate cardiac autophagy in obese diabetic mice
Pires, K. M. P., Buffolo, M., Schaaf, C., Symons, J. D., Cox, J. E., Abel, E. D., Selzman, C. H., & Boudina, S. (2017) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2017.10.001 · Cited by 39
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MethodSelf-citation
Antioxidant treatment normalizes mitochondrial energetics and myocardial insulin sensitivity independently of changes in systemic metabolic homeostasis in a mouse model of the metabolic syndrome
Ilkun, O. L., Wilde, N., Tuinei, J., Pires, K. M. P., Zhu, Y., Bugger, H., Soto, J. E., Wayment, B. E., Olsen, C. D., Litwin, S. E., et al. (2015) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2015.05.012 · Cited by 39
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BackgroundMethodSelf-citation
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Self-citation
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“For the measurement of oxygen consumption in permeabilized cardiac ﬁ bers, left ventricular (LV) subendocardial muscle ﬁ bers were used to measure oxygen consumption rates and ATP synthesis as previously described (Boudina et al, 2005).”
Self-citation
Overexpression of nuclear receptor SHP in adipose tissues affects diet-induced obesity and adaptive thermogenesis
Tabbi‐Anneni, I., Cooksey, R. C., Gunda, V., Liu, S., Mueller, A., Song, G., McClain, D. A., & Wang, L. (2010) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00655.2009 · Cited by 35
“In pathophysiological states where fatty acid availability is high, excess lipid oxidation or storage leads ultimately to an overproduction of reactive oxygen species, associated with increased mitochondrial uncoupling and energy dissipation (1, 4, 7).”
Background
Respirometric Oxidative Phosphorylation Assessment in Saponin-permeabilized Cardiac Fibers
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miR‐340‐5p Mediates Cardiomyocyte Oxidative Stress in Diabetes‐Induced Cardiac Dysfunction by Targeting Mcl‐1
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“The total ATP contents of the samples were determined using Luminescent ATP Detection Assay Kit (ab113849, Abcam) following the manufacturer ’ s instructions and the ATP synthesis, and ATP to O ratio was calculated as described [20].”
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“Likewise, reduced mitochondrial respiration has been reported both in db/ db mouse hearts (Boudina et al. 2007; Tocchetti et al. 2012) and ob/ob mouse hearts (Boudina et al. 2005).”
Background
Rescue of myocardial energetic dysfunction in diabetes through the correction of mitochondrial hyperacetylation by honokiol
Kerr, M. J., Miller, J. J. J. J., Thapa, D., Stiewe, S., Timm, K. N., Aparicio, C. N. M., Scott, I., Tyler, D. J., & Heather, L. C. (2020) · JCI Insight · doi:10.1172/jci.insight.140326 · Cited by 35
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Targeting Rab7‐Rilp Mediated Microlipophagy Alleviates Lipid Toxicity in Diabetic Cardiomyopathy
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Background
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“Perturbations in cardiac fatty acid composition may lead to defects in ion channel function, decreases in mitochondrial oxidative capacity, and rhythm disturbances [13-16].”
Background
The complexities of diabetic cardiomyopathy: Lessons from patients and animal models
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“Impaired ATP production T1DM, T2DM STZ-treated SD rats [43], db/db mice [ 48 ]”
Method
Myocardial mitochondrial dysfunction in mice lacking adiponectin receptor 1
Koentges, C., König, A., Pfeil, K., Hölscher, M. E., Schnick, T., Wende, A. R., Schrepper, A., Cimolai, M. C., Kersting, S., Hoffmann, M. M., et al. (2015) · Basic Research in Cardiology · doi:10.1007/s00395-015-0495-4 · Cited by 33
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Structural and Metabolic Effects of Obesity on the Myocardium and the Aorta
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Protocatechuic acid protects brain mitochondrial function in streptozotocin-induced diabetic rats
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Honokiol regulates mitochondrial substrate utilization and cellular fatty acid metabolism in diabetic mice heart
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Diabetic cardiomyopathy: the need for adjusting experimental models to meet clinical reality
Lezoualc’h, F., Badimón, L., Baker, H. E., Bernard, M., Czibik, G., de Boer, R. A., d’Humières, T., Kergoat, M., Kowala, M. C., Rieusset, J., et al. (2022) · Cardiovascular Research · doi:10.1093/cvr/cvac152 · Cited by 29
Cardiospecific CD36 suppression by lentivirus-mediated RNA interference prevents cardiac hypertrophy and systolic dysfunction in high-fat-diet induced obese mice
Zhang, Y., Bao, M., Dai, M., Wang, X., He, W., Tan, T., Lin, D., Wang, W., Wen, Y. R., & Zhang, R. (2015) · Cardiovascular Diabetology · doi:10.1186/s12933-015-0234-z · Cited by 33
Myocardial fatty acid utilization as a determinant of cardiac efficiency and function
Jaswal, J. S., & Ussher, J. R. (2009) · Clinical Lipidology · doi:10.2217/clp.09.18 · Cited by 29
A small molecule activator of AKT does not reduce ischemic injury of the rat heart
Moreira, J. M. A., Wohlwend, M., Alves, M. N. M., Wisløff, U., & Bye, A. (2015) · Journal of Translational Medicine · doi:10.1186/s12967-015-0444-x · Cited by 29
“Activity of citrate synthase and 3-hydroxyacylCoA dehydrogenase (HADH) were analyzed with colorimetric assays, as previously described [18].”
Method
Left ventricular vascular and metabolic adaptations to high‐intensity interval and moderate intensity continuous training: a randomized trial in healthy middle‐aged men
Eskelinen, J., HEINONEN, I. H. A., Löyttyniemi, E., Hakala, J. O., Heiskanen, M. A., Motiani, K. K., Virtanen, K. A., Pärkkä, J. P., Knuuti, J. M., Hannukainen, J. C., et al. (2016) · The Journal of Physiology · doi:10.1113/jp273089 · Cited by 29
“Interestingly, increased oxidative stress has been linked with impaired myocardial insulin sensitivity in previous studies (Boudina et al. 2005; Boudina et al. 2009) and, recently, it was shown that anti-oxidant treatment alleviates the impaired myocardial insulin sensitivity in rats (Ilkun et al.”
Proteomics of the Rat Myocardium during Development of Type 2 Diabetes Mellitus Reveals Progressive Alterations in Major Metabolic Pathways
Edhager, A. V., Povlsen, J. A., Løfgren, B., Bøtker, H. E., & Palmfeldt, J. (2018) · Journal of Proteome Research · doi:10.1021/acs.jproteome.8b00276 · Cited by 31
Risk stratification for cardiac death in hemodialysis patients without obstructive coronary artery disease
Nishimura, M., Tsukamoto, K., Tamaki, N., Kikuchi, K., Iwamoto, N., & Ono, T. (2010) · Kidney International · doi:10.1038/ki.2010.392 · Cited by 29
Targeting caveolin-3 for the treatment of diabetic cardiomyopathy
Murfitt, L., Whiteley, G., Iqbal, M. M., & Kitmitto, A. (2015) · Pharmacology & Therapeutics · doi:10.1016/j.pharmthera.2015.03.002 · Cited by 29
“, 2012) the ob/ob mouse (Christoffersen et al., 2003; Boudina et al., 2005), the Zucker Diabetic Fatty (ZDF) rat (Paradise et al.”
Background
Myocardial Fatty Acid Metabolism and Lipotoxicity in the Setting of Insulin Resistance
Kok, B. P., & Brindley, D. N. (2012) · Heart Failure Clinics · doi:10.1016/j.hfc.2012.06.008 · Cited by 29
High-fat diet improves tolerance to myocardial ischemia by delaying normalization of intracellular PH at reperfusion
Inserte, J., Aluja, D., Barba, I., Ruiz‐Meana, M., Miró‐Casas, E., Poncelas, M., Vilardosa, Ú., Castellano, J., & David Garcia-dorado, A. (2019) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2019.06.001 · Cited by 28
Fructose Metabolism and Cardiac Metabolic Stress
Annandale, M., Daniels, L. J., Li, X., Neale, J. P. H., Chau, A. H. L., Ambalawanar, H. A., James, S. L., Koutsifeli, P., Delbridge, L. M. D., & Mellor, K. M. (2021) · Frontiers in Pharmacology · doi:10.3389/fphar.2021.695486 · Cited by 29
“Impaired cardiac mitochondrial function is a common feature of diabetic cardiomyopathy (Diamant et al., 2003; Boudina et al., 2005; Anderson et al., 2009; Pham et al., 2014), but no studies to date have directly investigated whether diabetic mitochondrial dysfunction is linked to cardiac fructose metabolism in vivo.”
Background
Phosphoinositide dependent protein kinase 1 is required for exercise-induced cardiac hypertrophy but not the associated mitochondrial adaptations
Noh, J., Wende, A. R., Olsen, C. D., Kim, B. J., Bevins, J., Zhu, Y., Zhang, Q., Riehle, C., & Abel, E. D. (2015) · Journal of Molecular and Cellular Cardiology · doi:10.1016/j.yjmcc.2015.10.015 · Cited by 28
“Total protein lysates were extracted from frozen hearts as described previously [21].”
MethodSelf-citation
Mitochondria as Potential Targets in Antidiabetic Therapy
Moreira, P. I., & Oliveira, C. R. (2011) · Handbook of experimental pharmacology · doi:10.1007/978-3-642-17214-4_14 · Cited by 27
“These perturbations resulted in decreased mitochondrial efficiency (uncoupling) and a reduced capacity to respond to increased cardiac workload (Boudina et al. 2005).”
Background
Proteomic analysis of mitochondrial proteins in a mouse model of type 2 diabetes
Essop, M. F., Chan, W. A., & Hattingh, S. (2011) · Cardiovascular journal of South Africa/Cardiovascular journal of Southern Africa · doi:10.5830/cvja-2010-058 · Cited by 27
“For example, previous studies reported mitochondrial dysfunction in the hearts of ob/ob and db/db transgenic mice, well-described rodent models of obesity and type 2 diabetes.(2,3) Here it was proposed that reduced peptide levels of mitochondrial respiratory chain complexes I, III and V in ob/ob mice, and lower expres…”
Cluster Differentiating 36 (CD36) Deficiency Attenuates Obesity-Associated Oxidative Stress in the Heart
Gharib, M., Tao, H., Fungwe, T. V., & Hajri, T. (2016) · PLoS ONE · doi:10.1371/journal.pone.0155611 · Cited by 28
Loss of FoxOs in muscle reveals sex-based differences in insulin sensitivity but mitigates diet-induced obesity
Penniman, C. M., Beltran, P. A. S., Bhardwaj, G., Junck, T. L., Jena, J., Poro, K., Hirshman, M. F., Goodyear, L. J., & O'Neill, B. T. (2019) · Molecular Metabolism · doi:10.1016/j.molmet.2019.10.001 · Cited by 27
“4 to measure citrate synthase and HADH activity, as previously described [25,26].”
MethodSelf-citation
Early impairment of contractility reserve in patients with insulin resistance in comparison with healthy subjects
Dessalvi, C. C., Nocco, S., Piano, D., Deidda, M., Cossu, E., Baroni, M. G., & Mercuro, G. G. (2013) · Cardiovascular Diabetology · doi:10.1186/1475-2840-12-66 · Cited by 26
“Moreover, alteration of the myocardial energetic metabolism caused by IR can lead to ATP production impairment [27-30].”
Background
Impaired contractile function and mitochondrial respiratory capacity in response to oxygen deprivation in a rat model of pre‐diabetes
Essop, M. F., Chan, W. Y. A., Valle, A., García-Palmer, F., & Toit, E. F. D. (2009) · Acta Physiologica · doi:10.1111/j.1748-1716.2009.02024.x · Cited by 26
“However, we propose that downregulation of several nuclear-encoded mitochondrial genes and/or reduced protein levels of mitochondrial respiratory chain complexes with type 2 diabetes animal models (Boudina et al. 2005) may be contributing factors to this process.”
Background
Titanium dioxide nanoparticle-induced dysfunction of cardiac hemodynamics is involved in cardiac inflammation in mice
Hong, F., Wu, N., Zhao, X., Tian, Y., Zhou, Y., Chen, T., Zhai, Y., & Ji, L. (2016) · Journal of Biomedical Materials Research Part A · doi:10.1002/jbm.a.35831 · Cited by 26
“59,60 In our studies, TiO 2 NPs resulted in reductions of Na 1 /K 1 -ATPase, Ca 2 1 /Mg 2 1 -ATPase, 26 and ATP in the heart (Fig.”
Very long‐chain acyl‐CoA dehydrogenase (VLCAD‐) deficiency–studies on treatment effects and long‐term outcomes in mouse models
Tucci, S. (2017) · Journal of Inherited Metabolic Disease · doi:10.1007/s10545-017-0016-8 · Cited by 26
“In addition, VLCAD−/− mice displayed an inverse relationship between enhanced myocardial glucose uptake, as revealed by FDG-PET analysis and a reduced PCr/ATP ratio similar to previous reports on cardiac substrate metabolism in hypertrophied hearts (Nascimben et al 2004; Boudina et al 2005).”
What are the Biochemical Mechanisms Responsible for Enhanced Fatty Acid Utilization by Perfused Hearts from Type 2 Diabetic db/db Mice?
Carley, A. N., & Severson, D. L. (2008) · Cardiovascular Drugs and Therapy · doi:10.1007/s10557-008-6088-9 · Cited by 26
“Similar results have been obtained with obese and insulin-resistant ob/ob hearts; UCP3 protein content was not increased in ob/ob hearts that did show enhanced rates of FA oxidation [37].”
Result
Statins enhance peroxisome proliferator-activated receptor γ coactivator-1α activity to regulate energy metabolism
Wang, W., & Wong, C. (2009) · Journal of Molecular Medicine · doi:10.1007/s00109-009-0561-1 · Cited by 27
“The experiment was performed as described previously [ 29 ].”
Method
ZIP7 contributes to the pathogenesis of diabetic cardiomyopathy by suppressing mitophagy in mouse hearts
Yang, N., Zhang, R., Zhang, H., Yu, Y., & Xu, Z. (2024) · Cardiovascular Diabetology · doi:10.1186/s12933-024-02499-2 · Cited by 25
Caloric restriction in leptin deficiency does not correct myocardial steatosis: failure to normalize PPARα/PGC1α and thermogenic glycerolipid/fatty acid cycling
Rame, J. E., Barouch, L. A., Sack, M. N., Lynn, E. G., Abu-Asab, M. S., Tsokos, M., Kern, S. J., Barb, J. J., Munson, P. J., Halushka, M. K., et al. (2011) · Physiological Genomics · doi:10.1152/physiolgenomics.00088.2010 · Cited by 25
PKCε promotes cardiac mitochondrial and metabolic adaptation to chronic hypobaric hypoxia by GSK3β inhibition
McCarthy, J., Lochner, A., Opie, L. H., Sack, M. N., & Essop, M. F. (2010) · Journal of Cellular Physiology · doi:10.1002/jcp.22592 · Cited by 25
Impaired Coronary and Renal Vascular Function in Spontaneously Type 2 Diabetic Leptin-Deficient Mice
Westergren, H. U., Grönros, J., Heinonen, S. E., Miliotis, T., Jennbacken, K., Sabirsh, A., Ericsson, A., Jönsson‐Rylander, A., Svedlund, S., & Gan, L. (2015) · PLoS ONE · doi:10.1371/journal.pone.0130648 · Cited by 25
Global transcriptional response of Saccharomyces cerevisiae to the deletion of SDH3
Cimini, D., Patil, K. R., Schiraldi, C., & Nielsen, J. (2009) · BMC Systems Biology · doi:10.1186/1752-0509-3-17 · Cited by 25
“Defects in the respiratory chain and related energy metabolism have been shown to be key factors in inducing several human diseases, including diabetes, obesity and certain types of cancers [2-6].”
Background
Mitochondrial DNA Variant for Complex I Reveals a Role in Diabetic Cardiac Remodeling
Sethumadhavan, S., Vasquez-Vivar, J. M., Migrino, R. Q., Harmann, L. M., Jacob, H. J., & Lazar, J. (2012) · Journal of Biological Chemistry · doi:10.1074/jbc.m111.327866 · Cited by 24
“Mitochondrial dysfunction appears to be an accompanying phenomenon via increased expression of uncoupling proteins and oxidative stress (23, 24).”
Background
Cardiac Response to Oxidative Stress Induced by Mitochondrial Dysfunction
Kim, H. K., Nilius, B., Kim, N., Ko, K. S., Rhee, B. D., & Han, J. (2016) · Reviews of physiology, biochemistry and pharmacology · doi:10.1007/112_2015_5004 · Cited by 26
“Taken together, these findings demonstrate the multiple roles of oxidative stress in the development of DCM.”
BackgroundInfluential
Eat and Death: Chronic Over-Eating
Engin, A. (2017) · Advances in experimental medicine and biology · doi:10.1007/978-3-319-48382-5_3 · Cited by 22
Mitochondrial function in heart failure: The impact of ischemic and non-ischemic etiology
Park, S., Trinity, J. D., Gifford, J. R., Diakos, N., McCreath, L., Drakos, S. G., & Richardson, R. S. (2016) · International Journal of Cardiology · doi:10.1016/j.ijcard.2016.06.147 · Cited by 23
“The proton motive force, the proton gradient between the matrix and the intermembrane space of the mitochondria, facilitates ATP production [41] and in combination with non-phosphorylating proton conductance regulates the kinetics and efficiency of mitochondrial respiration [7,16].”
Background
Melatonin Efficacy in Obese Leptin-Deficient Mice Heart
Stacchiotti, A., Favero, G., Giugno, L., Golic, I., Korac, A., & Rezzani, R. (2017) · Nutrients · doi:10.3390/nu9121323 · Cited by 25
“Given that heart is the most mitochondria-rich organ of the body and bases on an oxidative metabolism, many studies reported that mitochondria morphology and function are impaired in cardiovascular diseases and obesity [22,42,43].”
Background
Diabetic Cardiomyopathy: What Clinicians Should Know
Smati, H., Qadeer, Y. K., Rodríguez, M., Moras, E., Fonarow, G. C., Isaacs, S. D., Marwick, T. H., & Krittanawong, C. (2024) · The American Journal of Medicine · doi:10.1016/j.amjmed.2024.10.026 · Cited by 23
Roxadustat improves diabetic myocardial injury by upregulating HIF-1α/UCP2 against oxidative stress
Fang, T., Ma, C., Yang, B., Zhao, M., Sun, L., & Zheng, N. (2025) · Cardiovascular Diabetology · doi:10.1186/s12933-025-02601-2 · Cited by 25
“In models of type 2 diabetes (Lep^db/db and ob/ob), myocardial tissues exhibit significantly reduced mitochondrial ATP synthesis, heightened oxidative stress, elevated ROS production, and structural damage [29– 30].”
Obesity Preserves Myocardial Function During Blockade of the Glycolytic Pathway
de Campos, D. H. S., Leopoldo, A. S., Lima‐Leopoldo, A. P., do Nascimento, A. F., de Oliveira-Junior, S. A., da Silva, D. C. T., Sugizaki, M. M., Padovani, C. R., & Cicogna, A. C. (2014) · Arquivos Brasileiros de Cardiologia · doi:10.5935/abc.20140135 · Cited by 23
The afterload-dependent peak efficiency of the isolated working rat heart is unaffected by streptozotocin-induced diabetes
Han, J., Goo, S., Barrett, C. J., Mellor, K. M., Taberner, A. J., & Loiselle, D. S. (2014) · Cardiovascular Diabetology · doi:10.1186/1475-2840-13-4 · Cited by 22
Exercise of obese mice induces cardioprotection and oxygen sparing in hearts exposed to high-fat load
Boardman, N. T., Hafstad, A. D., Lund, J., Rossvoll, L., & Aasum, E. (2017) · American Journal of Physiology-Heart and Circulatory Physiology · doi:10.1152/ajpheart.00382.2017 · Cited by 22
“Although chronic hyperlipidemia may contribute to the progression of impaired myocardial Ca2 handling in diabetes, some studies have reported that, by adding FAs (which is often absent when studying isolated cell preparations), cardiomyocytes from diabetic/obese hearts show improved Ca2 handling and contractile functi…”
BackgroundMethodInfluential
Sex Differences in Cardiac Mitochondria in the New Zealand Obese Mouse
John, C., Grune, J., Ott, C., Nowotny, K., Deubel, S., Kühne, A., Schubert, C., Kintscher, U., Regitz‐Zagrosek, V., & Grune, T. (2018) · Frontiers in Endocrinology · doi:10.3389/fendo.2018.00732 · Cited by 22
“Interestingly, investigations in other obesity mouse models related to T2DM, such as the ob/ob and the db/db mice, showed likewise decreased cardiac mitochondrial respiration capacity and lower expression of respiration chain complexes (42, 43).”
Cellular Protein Quality Control in Diabetic Cardiomyopathy: From Bench to Bedside
Kaur, N., Raja, R., Ruiz‐Velasco, A., & Liu, W. (2020) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2020.585309 · Cited by 24
Low intrinsic aerobic exercise capacity and systemic insulin resistance are not associated with changes in myocardial substrate oxidation or insulin sensitivity
Schwarzer, M., Britton, S. L., Koch, L. G., Wisløff, U., & Doenst, T. (2010) · Basic Research in Cardiology · doi:10.1007/s00395-010-0087-2 · Cited by 23
“[3] established a link between systemic insulin resistance, fatty acid overload, cardiac mitochondrial dysfunction, and diabetic cardiomyopathy in db/db mice.”
Mitochondrial Reactive Oxygen Species Dysregulation in Heart Failure with Preserved Ejection Fraction: A Fraction of the Whole
Martinez, C. S., Zheng, A., & Xiao, Q. (2024) · Antioxidants · doi:10.3390/antiox13111330 · Cited by 26
Mitochondrial Quality Control Mechanisms during Diabetic Cardiomyopathy
Ketenci, M., Zablocki, D., & Sadoshima, J. (2022) · JMA Journal · doi:10.31662/jmaj.2022-0155 · Cited by 21

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.
ORCID: Boudina, Sihem
Young, Martin E.
Abel, E. Dale
Venue: Circulation
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2005-10-25
Volume: 112
Issue: 17
Pages: 2686-2695
ISSN: 0009-7322 (ISSN-L)
1524-4539
DOI: 10.1161/circulationaha.105.554360
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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Reduced Mitochondrial Oxidative Capacity and Increased Mitochondrial Uncoupling Impair Myocardial Energetics in Obesity

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