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  • 1
    Online Resource
    Online Resource
    Myocardial Fatty Acid Metabolism in Health and Disease
    American Physiological Society ; 2010
    In:  Physiological Reviews Vol. 90, No. 1 ( 2010-01), p. 207-258
    Details
    In: Physiological Reviews, American Physiological Society, Vol. 90, No. 1 ( 2010-01), p. 207-258
    Abstract: There is a constant high demand for energy to sustain the continuous contractile activity of the heart, which is met primarily by the β-oxidation of long-chain fatty acids. The control of fatty acid β-oxidation is complex and is aimed at ensuring that the supply and oxidation of the fatty acids is sufficient to meet the energy demands of the heart. The metabolism of fatty acids via β-oxidation is not regulated in isolation; rather, it occurs in response to alterations in contractile work, the presence of competing substrates (i.e., glucose, lactate, ketones, amino acids), changes in hormonal milieu, and limitations in oxygen supply. Alterations in fatty acid metabolism can contribute to cardiac pathology. For instance, the excessive uptake and β-oxidation of fatty acids in obesity and diabetes can compromise cardiac function. Furthermore, alterations in fatty acid β-oxidation both during and after ischemia and in the failing heart can also contribute to cardiac pathology. This paper reviews the regulation of myocardial fatty acid β-oxidation and how alterations in fatty acid β-oxidation can contribute to heart disease. The implications of inhibiting fatty acid β-oxidation as a potential novel therapeutic approach for the treatment of various forms of heart disease are also discussed.
    Type of Medium: Online Resource
    ISSN: 0031-9333 , 1522-1210
    URL: Article
    DOI: 10.1152/physrev.00015.2009
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 1471693-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Impaired Myocardial Fatty Acid Oxidation and Reduced Protein Expression of Retinoid X Receptor-α in Pacing-Induced Heart Failure
    Ovid Technologies (Wolters Kluwer Health) ; 2002
    In:  Circulation Vol. 106, No. 5 ( 2002-07-30), p. 606-612
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 106, No. 5 ( 2002-07-30), p. 606-612
    Abstract: Background — The nuclear receptors peroxisome proliferator-activated receptor-α (PPARα) and retinoid X receptor α (RXRα) stimulate the expression of key enzymes of free fatty acid (FFA) oxidation. We tested the hypothesis that the altered metabolic phenotype of the failing heart involves changes in the protein expression of PPARα and RXRα. Methods and Results — Cardiac substrate uptake and oxidation were measured in 8 conscious, chronically instrumented dogs with decompensated pacing-induced heart failure and in 8 normal dogs by infusing 3 isotopically labeled substrates: 3 H-oleate, 14 C-glucose, and 13 C-lactate. Although myocardial O 2 consumption was not different between the 2 groups, the rate of oxidation of FFA was lower (2.8±0.6 versus 4.7±0.3 μmol · min −1 · 100g −1 ) and of glucose was higher (4.6±1.0 versus 1.8±0.5 μmol · min −1 · 100g −1 ) in failing compared with normal hearts ( P 〈 0.05). The rates of lactate uptake and lactate output were not significantly different between the 2 groups. In left ventricular tissue from failing hearts, the activity of 2 key enzymes of FFA oxidation was significantly reduced: carnitine palmitoyl transferase-I (0.54±0.04 versus 0.66±0.04 μmol · min −1 · g −1 ) and medium chain acyl-coenzyme A dehydrogenase (MCAD; 1.8±0.1 versus 2.9±0.3 μmol · min −1 · g −1 ). Consistently, the protein expression of MCAD and of RXRα were significantly reduced by 38% in failing hearts, but the expression of PPARα was not different. Moreover, there were significant correlations between the expression of RXRα and the expression and activity of MCAD. Conclusions — Our results provide the first evidence for a link between the reduced expression of RXRα and the switch in metabolic phenotype in severe heart failure.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.0000023531.22727.C1
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2002
    detail.hit.zdb_id: 1466401-X
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  • 3
    Online Resource
    Online Resource
    Glucose Metabolism in the Ischemic Heart
    Ovid Technologies (Wolters Kluwer Health) ; 1997
    In:  Circulation Vol. 95, No. 2 ( 1997-01-21), p. 313-315
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 95, No. 2 ( 1997-01-21), p. 313-315
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.95.2.313
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1997
    detail.hit.zdb_id: 1466401-X
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  • 4
    Online Resource
    Online Resource
    Malonyl-CoA Decarboxylase Inhibition as a Novel Approach to Treat Ischemic Heart Disease
    Springer Science and Business Media LLC ; 2006
    In:  Cardiovascular Drugs and Therapy Vol. 20, No. 6 ( 2006-12), p. 433-439
    Details
    In: Cardiovascular Drugs and Therapy, Springer Science and Business Media LLC, Vol. 20, No. 6 ( 2006-12), p. 433-439
    Type of Medium: Online Resource
    ISSN: 0920-3206 , 1573-7241
    URL: Article
    DOI: 10.1007/s10557-006-0634-0
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2006
    detail.hit.zdb_id: 2003553-6
    SSG: 15,3
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  • 5
    Online Resource
    Online Resource
    Regulation of cardiac malonyl-CoA content and fatty acid oxidation during increased cardiac power
    American Physiological Society ; 2005
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 289, No. 3 ( 2005-09), p. H1033-H1037
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 289, No. 3 ( 2005-09), p. H1033-H1037
    Abstract: Myocardial fatty acid oxidation is regulated by carnitine palmitoyltransferase I (CPT I), which is inhibited by malonyl-CoA. Increased cardiac power causes a fall in malonyl-CoA content and accelerated fatty acid oxidation; however, the mechanism for the decrease in malonyl-CoA is unclear. Malonyl-CoA is formed by acetyl-CoA carboxylase (ACC) and degraded by malonyl-CoA decarboxylase (MCD); thus a fall in malonyl-CoA could be due to activation of MCD, inhibition of ACC, or both. This study assessed the effects of increased cardiac power on malonyl-CoA content and ACC and MCD activities. Anesthetized pigs were studied under control conditions and during increased cardiac power in response to dobutamine infusion and aortic constriction alone, under hyperglycemic conditions, or with the CPT I inhibitor oxfenicine. An increase in cardiac power was accompanied by increased myocardial O 2 consumption, decreased malonyl-CoA concentration, and increased fatty acid oxidation. There were no differences among groups in activity of ACC or AMP-activated protein kinase (AMPK), which physiologically inhibits ACC. There also were no differences in V max or K m of MCD. Previous studies have demonstrated that AMPK can be inhibited by protein kinase B (PKB); however, PKB was activated by dobutamine and the elevated insulin that accompanied hyperglycemia, but there was no effect on AMPK activity. In conclusion, the fall in malonyl-CoA and increase in fatty acid oxidization that occur with increased cardiac work were not due to inhibition of ACC or activation of MCD, suggesting alternative regulatory mechanisms for the work-induced decrease in malonyl-CoA concentration.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00210.2005
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2005
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Regulation of Malonyl-CoA Concentration and Turnover in the Normal Heart
    Elsevier BV ; 2004
    In:  Journal of Biological Chemistry Vol. 279, No. 33 ( 2004-08), p. 34298-34301
    Details
    In: Journal of Biological Chemistry, Elsevier BV, Vol. 279, No. 33 ( 2004-08), p. 34298-34301
    Type of Medium: Online Resource
    ISSN: 0021-9258
    URL: Article
    DOI: 10.1074/jbc.M405488200
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2004
    detail.hit.zdb_id: 2141744-1
    detail.hit.zdb_id: 1474604-9
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Transient activation of P38 MAP kinase and up-regulation of Pim-1 kinase in cardiac hypertrophy despite no activation of AMPK
    Elsevier BV ; 2008
    In:  Journal of Molecular and Cellular Cardiology Vol. 45, No. 3 ( 2008-09), p. 404-410
    Details
    In: Journal of Molecular and Cellular Cardiology, Elsevier BV, Vol. 45, No. 3 ( 2008-09), p. 404-410
    Type of Medium: Online Resource
    ISSN: 0022-2828
    URL: Article
    DOI: 10.1016/j.yjmcc.2008.06.008
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2008
    detail.hit.zdb_id: 1469767-1
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  • 8
    Online Resource
    Online Resource
    Cardiac Energy Metabolism in Obesity
    Ovid Technologies (Wolters Kluwer Health) ; 2007
    In:  Circulation Research Vol. 101, No. 4 ( 2007-08-17), p. 335-347
    Details
    In: Circulation Research, Ovid Technologies (Wolters Kluwer Health), Vol. 101, No. 4 ( 2007-08-17), p. 335-347
    Abstract: Obesity results in marked alterations in cardiac energy metabolism, with a prominent effect being an increase in fatty acid uptake and oxidation by the heart. Obesity also results in dramatic changes in the release of adipokines, such as leptin and adiponectin, both of which have emerged as important regulators of cardiac energy metabolism. The link among obesity, cardiovascular disease, lipid metabolism, and adipokine signaling is complex and not well understood. However, optimizing cardiac energy metabolism in obese subjects may be one approach to preventing and treating cardiac dysfunction that can develop in this population. This review discusses what is presently known about the effects of obesity and the impact adipokines have on cardiac energy metabolism and insulin signaling. The clinical implications of obesity and energy metabolism on cardiac disease are also discussed.
    Type of Medium: Online Resource
    ISSN: 0009-7330 , 1524-4571
    URL: Article
    DOI: 10.1161/CIRCRESAHA.107.150417
    RVK:
    XA 10000
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2007
    detail.hit.zdb_id: 1467838-X
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  • 9
    Online Resource
    Online Resource
    Myocardial Substrate Metabolism in the Normal and Failing Heart
    American Physiological Society ; 2005
    In:  Physiological Reviews Vol. 85, No. 3 ( 2005-07), p. 1093-1129
    Details
    In: Physiological Reviews, American Physiological Society, Vol. 85, No. 3 ( 2005-07), p. 1093-1129
    Abstract: The alterations in myocardial energy substrate metabolism that occur in heart failure, and the causes and consequences of these abnormalities, are poorly understood. There is evidence to suggest that impaired substrate metabolism contributes to contractile dysfunction and to the progressive left ventricular remodeling that are characteristic of the heart failure state. The general concept that has recently emerged is that myocardial substrate selection is relatively normal during the early stages of heart failure; however, in the advanced stages there is a downregulation in fatty acid oxidation, increased glycolysis and glucose oxidation, reduced respiratory chain activity, and an impaired reserve for mitochondrial oxidative flux. This review discusses 1) the metabolic changes that occur in chronic heart failure, with emphasis on the mechanisms that regulate the changes in the expression of metabolic genes and the function of metabolic pathways; 2) the consequences of these metabolic changes on cardiac function; 3) the role of changes in myocardial substrate metabolism on ventricular remodeling and disease progression; and 4) the therapeutic potential of acute and long-term manipulation of cardiac substrate metabolism in heart failure.
    Type of Medium: Online Resource
    ISSN: 0031-9333 , 1522-1210
    URL: Article
    DOI: 10.1152/physrev.00006.2004
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2005
    detail.hit.zdb_id: 1471693-8
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    Malonyl-CoA decarboxylase inhibition suppresses fatty acid oxidation and reduces lactate production during demand-induced ischemia
    American Physiological Society ; 2005
    In:  American Journal of Physiology-Heart and Circulatory Physiology Vol. 289, No. 6 ( 2005-12), p. H2304-H2309
    Details
    In: American Journal of Physiology-Heart and Circulatory Physiology, American Physiological Society, Vol. 289, No. 6 ( 2005-12), p. H2304-H2309
    Abstract: The rate of cardiac fatty acid oxidation is regulated by the activity of carnitine palmitoyltransferase-I (CPT-I), which is inhibited by malonyl-CoA. We tested the hypothesis that the activity of the enzyme responsible for malonyl-CoA degradation, malonyl-CoA decarboxlyase (MCD), regulates myocardial malonyl-CoA content and the rate of fatty acid oxidation during demand-induced ischemia in vivo. The myocardial content of malonyl-CoA was increased in anesthetized pigs using a specific inhibitor of MCD (CBM-301106), which we hypothesized would result in inhibition of CPT-I, reduction in fatty acid oxidation, a reciprocal activation of glucose oxidation, and diminished lactate production during demand-induced ischemia. Under normal-flow conditions, treatment with the MCD inhibitor significantly reduced oxidation of exogenous fatty acids by 82%, shifted the relationship between arterial fatty acids and fatty acid oxidation downward, and increased glucose oxidation by 50%. Ischemia was induced by a 20% flow reduction and β-adrenergic stimulation, which resulted in myocardial lactate production. During ischemia MCD inhibition elevated malonyl-CoA content fourfold, reduced free fatty acid oxidation rate by 87%, and resulted in a 50% decrease in lactate production. Moreover, fatty acid oxidation during ischemia was inversely related to the tissue malonyl-CoA content ( r = −0.63). There were no differences between groups in myocardial ATP content, the activity of pyruvate dehydrogenase, or myocardial contractile function during ischemia. Thus modulation of MCD activity is an effective means of regulating myocardial fatty acid oxidation under normal and ischemic conditions and reducing lactate production during demand-induced ischemia.
    Type of Medium: Online Resource
    ISSN: 0363-6135 , 1522-1539
    URL: Article
    DOI: 10.1152/ajpheart.00599.2005
    RVK:
    WA 15000
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2005
    detail.hit.zdb_id: 1477308-9
    SSG: 12
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