title: Triacylglycerol turnover in the failing heart.
abstract: No longer regarded as physiologically inert the endogenous triacylglyceride (TAG) pool within the cardiomyocyte is now recognized to play a dynamic role in metabolic regulation. Beyond static measures of content, the relative rates of interconversion among acyl intermediates are more closely linked to dynamic processes of physiological function in normal and diseased hearts, with the potential for both adaptive and maladaptive contributions. Indeed, multiple inefficiencies in cardiac metabolism have been identified in the decompensated, hypertrophied and failing heart. Among the intracellular responses to physiological, metabolic and pathological stresses, TAG plays a central role in the balance of lipid handling and signaling mechanisms. TAG dynamics are profoundly altered from normal in both diabetic and pathologically stressed hearts. More than just expansion or contraction of the stored lipid pool, the turnover rates of TAG are sensitive to and compete against other enzymatic pathways, anabolic and catabolic, for reactive acyl-CoA units. The rates of TAG synthesis and lipolysis thusly affect multiple components of cardiomyocyte function, including energy metabolism, cell signaling, and enzyme activation, as well as the regulation of gene expression in both normal and diseased states. This review examines the multiple etiologies and metabolic consequences of the failing heart and the central role of lipid storage dynamics in the pathogenic process. This article is part of a Special Issue entitled: Heart Lipid Metabolism edited by G.D. Lopaschuk.
authors.affiliation: Sanford Burnham Prebys Medical Discovery Institute, Orlando, FL, United States.
authors.forename: Andrew N
authors.initials: AN
authors.lastname: Carley
authors.affiliation: Sanford Burnham Prebys Medical Discovery Institute, Orlando, FL, United States. Electronic address: dougl@sbpdiscovery.org.
authors.forename: E Douglas
authors.initials: ED
authors.lastname: Lewandowski
mesh_terms: D000818:Animals; D005227:Fatty Acids / Q000378:metabolism; D006333:Heart Failure / Q000378:metabolism*; D006801:Humans; D008928:Mitochondria / Q000378:metabolism; D010084:Oxidation-Reduction; D015398:Signal Transduction; D014280:Triglycerides / Q000378:metabolism*
chemical_list: D005227:Fatty Acids; D014280:Triglycerides
keywords: Diabetes; Fatty acids; Heart failure; Hypertrophy; Metabolism; Triglyceride