Myocardial substrate metabolism in obesity

Obesity is linked to a wide variety of cardiac changes, from subclinical diastolic dysfunction to end-stage systolic heart failure. Obesity causes changes in cardiac metabolism, which make ATP production and utilization less efficient, producing functional consequences that are linked to the increas...

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Main Authors: Rider, O, Cox, P, Tyler, D, Clarke, K, Neubauer, S
Format: Journal article
Published: Nature Publishing Group 2012
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author Rider, O
Cox, P
Tyler, D
Clarke, K
Neubauer, S
author_facet Rider, O
Cox, P
Tyler, D
Clarke, K
Neubauer, S
author_sort Rider, O
collection OXFORD
description Obesity is linked to a wide variety of cardiac changes, from subclinical diastolic dysfunction to end-stage systolic heart failure. Obesity causes changes in cardiac metabolism, which make ATP production and utilization less efficient, producing functional consequences that are linked to the increased rate of heart failure in this population. As a result of the increases in circulating fatty acids and insulin resistance that accompanies excess fat storage, several of the proteins and genes that are responsible for fatty acid uptake and metabolism are upregulated, and the metabolic machinery responsible for glucose utilization and oxidation are inhibited. The resultant increase in fatty acid metabolism, and the inherent alterations in the proteins of the electron transport chain used to create the gradient needed to drive mitochondrial ATP production, results in a decrease in efficiency of cardiac work and a relative increase in oxygen usage. These changes in cardiac mitochondrial metabolism are potential therapeutic targets for the treatment and prevention of obesity-related heart failure. © 2013 Macmillan Publishers Limited.
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spelling oxford-uuid:8cbdbe53-c81c-4347-8ea4-35c58bee87932022-03-26T22:46:31ZMyocardial substrate metabolism in obesityJournal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:8cbdbe53-c81c-4347-8ea4-35c58bee8793Symplectic Elements at OxfordNature Publishing Group2012Rider, OCox, PTyler, DClarke, KNeubauer, SObesity is linked to a wide variety of cardiac changes, from subclinical diastolic dysfunction to end-stage systolic heart failure. Obesity causes changes in cardiac metabolism, which make ATP production and utilization less efficient, producing functional consequences that are linked to the increased rate of heart failure in this population. As a result of the increases in circulating fatty acids and insulin resistance that accompanies excess fat storage, several of the proteins and genes that are responsible for fatty acid uptake and metabolism are upregulated, and the metabolic machinery responsible for glucose utilization and oxidation are inhibited. The resultant increase in fatty acid metabolism, and the inherent alterations in the proteins of the electron transport chain used to create the gradient needed to drive mitochondrial ATP production, results in a decrease in efficiency of cardiac work and a relative increase in oxygen usage. These changes in cardiac mitochondrial metabolism are potential therapeutic targets for the treatment and prevention of obesity-related heart failure. © 2013 Macmillan Publishers Limited.
spellingShingle Rider, O
Cox, P
Tyler, D
Clarke, K
Neubauer, S
Myocardial substrate metabolism in obesity
title Myocardial substrate metabolism in obesity
title_full Myocardial substrate metabolism in obesity
title_fullStr Myocardial substrate metabolism in obesity
title_full_unstemmed Myocardial substrate metabolism in obesity
title_short Myocardial substrate metabolism in obesity
title_sort myocardial substrate metabolism in obesity
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AT coxp myocardialsubstratemetabolisminobesity
AT tylerd myocardialsubstratemetabolisminobesity
AT clarkek myocardialsubstratemetabolisminobesity
AT neubauers myocardialsubstratemetabolisminobesity