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Article: Metabolic response to an acute jump in cardiac workload: Effects on malonyl-CoA, mechanical efficiency, and fatty acid oxidation

TitleMetabolic response to an acute jump in cardiac workload: Effects on malonyl-CoA, mechanical efficiency, and fatty acid oxidation
Authors
Issue Date2008
Citation
American Journal of Physiology - Heart and Circulatory Physiology, 2008, v. 294 n. 2, p. H954-H960 How to Cite?
AbstractInhibition of myocardial fatty acid oxidation can improve left ventricular (LV) mechanical efficiency by increasing LV power for a given rate of myocardial energy expenditure. This phenomenon has not been assessed at high workloads in nonischemic myocardium; therefore, we subjected in vivo pig hearts to a high workload for 5 min and assessed whether blocking mitochondrial fatty acid oxidation with the carnitine palmitoyltransferase-I inhibitor oxfenicine would improve LV mechanical efficiency. In addition, the cardiac content of malonyl-CoA (an endogenous inhibitor of carnitine palmitoyltransferase-I) and activity of acetyl-CoA carboxylase (which synthesizes malonyl-CoA) were assessed. Increased workload was induced by aortic constriction and dobutamine infusion, and LV efficiency was calculated from the LV pressure-volume loop and LV energy expenditure. In untreated pigs, the increase in LV power resulted in a 2.5-fold increase in fatty acid oxidation and cardiac malonyl-CoA content but did not affect the activation state of acetyl-CoA carboxylase. The activation state of the acetyl-CoA carboxylase inhibitory kinase AMP-activated protein kinase decreased by 40% with increased cardiac workload. Pretreatment with oxfenicine inhibited fatty acid oxidation by 75% and had no effect on cardiac energy expenditure but significantly increased LV power and LV efficiency (37 ± 5% vs. 26 ± 5%, P < 0.05) at high workload. In conclusion, 1) myocardial fatty acid oxidation increases with a short-term increase in cardiac workload, despite an increase in malonyl-CoA concentration, and 2) inhibition of fatty acid oxidation improves LV mechanical efficiency by increasing LV power without affecting cardiac energy expenditure. Copyright © 2008 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/195864
ISSN
2015 Impact Factor: 3.324
2015 SCImago Journal Rankings: 1.823
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorZhou, L-
dc.contributor.authorHuang, H-
dc.contributor.authorYuan, CL-
dc.contributor.authorKeung, W-
dc.contributor.authorLopaschuk, GD-
dc.contributor.authorStanley, WC-
dc.date.accessioned2014-03-19T01:46:11Z-
dc.date.available2014-03-19T01:46:11Z-
dc.date.issued2008-
dc.identifier.citationAmerican Journal of Physiology - Heart and Circulatory Physiology, 2008, v. 294 n. 2, p. H954-H960-
dc.identifier.issn0363-6135-
dc.identifier.urihttp://hdl.handle.net/10722/195864-
dc.description.abstractInhibition of myocardial fatty acid oxidation can improve left ventricular (LV) mechanical efficiency by increasing LV power for a given rate of myocardial energy expenditure. This phenomenon has not been assessed at high workloads in nonischemic myocardium; therefore, we subjected in vivo pig hearts to a high workload for 5 min and assessed whether blocking mitochondrial fatty acid oxidation with the carnitine palmitoyltransferase-I inhibitor oxfenicine would improve LV mechanical efficiency. In addition, the cardiac content of malonyl-CoA (an endogenous inhibitor of carnitine palmitoyltransferase-I) and activity of acetyl-CoA carboxylase (which synthesizes malonyl-CoA) were assessed. Increased workload was induced by aortic constriction and dobutamine infusion, and LV efficiency was calculated from the LV pressure-volume loop and LV energy expenditure. In untreated pigs, the increase in LV power resulted in a 2.5-fold increase in fatty acid oxidation and cardiac malonyl-CoA content but did not affect the activation state of acetyl-CoA carboxylase. The activation state of the acetyl-CoA carboxylase inhibitory kinase AMP-activated protein kinase decreased by 40% with increased cardiac workload. Pretreatment with oxfenicine inhibited fatty acid oxidation by 75% and had no effect on cardiac energy expenditure but significantly increased LV power and LV efficiency (37 ± 5% vs. 26 ± 5%, P < 0.05) at high workload. In conclusion, 1) myocardial fatty acid oxidation increases with a short-term increase in cardiac workload, despite an increase in malonyl-CoA concentration, and 2) inhibition of fatty acid oxidation improves LV mechanical efficiency by increasing LV power without affecting cardiac energy expenditure. Copyright © 2008 the American Physiological Society.-
dc.languageeng-
dc.relation.ispartofAmerican Journal of Physiology - Heart and Circulatory Physiology-
dc.titleMetabolic response to an acute jump in cardiac workload: Effects on malonyl-CoA, mechanical efficiency, and fatty acid oxidation-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1152/ajpheart.00557.2007-
dc.identifier.pmid18083904-
dc.identifier.scopuseid_2-s2.0-39149093398-
dc.identifier.volume294-
dc.identifier.issue2-
dc.identifier.spageH954-
dc.identifier.epageH960-
dc.identifier.isiWOS:000253072400048-

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