Cardiovascular Research Advance Access originally published online on May 31, 2008
Cardiovascular Research 2008 79(2):205-207; doi:10.1093/cvr/cvn134
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Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2008. For permissions please email: journals.permissions@oxfordjournals.org
Signalling in cardiac metabolism
1 Cardiovascular Research Group, University of Alberta, 423 Heritage Medical Research Center, Edmonton, Alberta, Canada T6G 2S2
2 Center for Cardiovascular Research, Washington University School of Medicine, St. Louis, Missouri, USA
* Corresponding author. Tel: +1 780 492 2170; fax: +1 780 492 9753. E-mail address: gary.lopaschuk@ualberta.ca
| The first 150 words of the full text of this article appear below. |
| 1. Introduction |
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The heart requires large amounts of energy to sustain contractile function, and is the major consumer of energy in the body on a weight basis. Energy reserves are limited in the heart, so energy in the form of adenosine triphosphate (ATP) must be produced continually by the catabolism of different energy carbon substrates. The heart is an omnivore and can use a number of different energy substrates, including fatty acids, glucose, lactate, pyruvate, ketones, and amino acids.1–4 Myocardial energy metabolism must be tightly regulated, as the heart cannot afford to produce either too little or too much ATP. In the normal healthy heart, almost all (>95%) of the ATP generated in the heart comes from mitochondrial oxidative phosphorylation, with the remainder being derived from glycolysis.1–4 Of these, fatty acids, glucose, and lactate normally make the greatest contribution to overall energy metabolism, primarily because the heart sees the highest concentration of
| 2. Control of myocardial mitochondrial function |
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| 3. Control of glycolysis |
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| 4. Signalling control of cardiac fatty acid metabolism |
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| 5. Exogenous hormonal and substrate control of cardiac energy metabolism |
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| 6. Conclusions |
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