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Evidence for Intramyocardial Disruption of Lipid Metabolism and Increased Myocardial Ketone Utilization in Advanced Human Heart Failure
Journal article   Open access

Evidence for Intramyocardial Disruption of Lipid Metabolism and Increased Myocardial Ketone Utilization in Advanced Human Heart Failure

Kenneth C Bedi, Jr, Nathaniel W Snyder, Jeffrey Brandimarto, Moez Aziz, Clementina Mesaros, Andrew J Worth, Linda L Wang, Ali Javaheri, Ian A Blair, Kenneth B Margulies, …
Circulation (New York, N.Y.), v 133(8), pp 706-716
23 Feb 2016
PMID: 26819374
url
https://doi.org/10.1161/circulationaha.115.017545View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze) Open
url
https://doi.org/10.1161/CIRCULATIONAHA.115.017545View
Published, Version of Record (VoR) Open

Abstract

Adult Aged Case-Control Studies Chronic Disease Disease Progression Female Heart Failure - diagnosis Heart Failure - metabolism Humans Ketones - metabolism Lipid Metabolism - physiology Male Middle Aged Myocardium - metabolism Myocardium - pathology ESI Highly Cited Paper (Incites)
The failing human heart is characterized by metabolic abnormalities, but these defects remains incompletely understood. In animal models of heart failure there is a switch from a predominance of fatty acid utilization to the more oxygen-sparing carbohydrate metabolism. Recent studies have reported decreases in myocardial lipid content, but the inclusion of diabetic and nondiabetic patients obscures the distinction of adaptations to metabolic derangements from adaptations to heart failure per se. We performed both unbiased and targeted myocardial lipid surveys using liquid chromatography-mass spectroscopy in nondiabetic, lean, predominantly nonischemic, advanced heart failure patients at the time of heart transplantation or left ventricular assist device implantation. We identified significantly decreased concentrations of the majority of myocardial lipid intermediates, including long-chain acylcarnitines, the primary subset of energetic lipid substrate for mitochondrial fatty acid oxidation. We report for the first time significantly reduced levels of intermediate and anaplerotic acyl-coenzyme A (CoA) species incorporated into the Krebs cycle, whereas the myocardial concentration of acetyl-CoA was significantly increased in end-stage heart failure. In contrast, we observed an increased abundance of ketogenic β-hydroxybutyryl-CoA, in association with increased myocardial utilization of β-hydroxybutyrate. We observed a significant increase in the expression of the gene encoding succinyl-CoA:3-oxoacid-CoA transferase, the rate-limiting enzyme for myocardial oxidation of β-hydroxybutyrate and acetoacetate. These findings indicate increased ketone utilization in the severely failing human heart independent of diabetes mellitus, and they support the role of ketone bodies as an alternative fuel and myocardial ketone oxidation as a key metabolic adaptation in the failing human heart.

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Highly Cited Paper 
Collaboration types
Domestic collaboration
Web of Science research areas
Cardiac & Cardiovascular Systems
Peripheral Vascular Disease
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