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Energy metabolism in heart failure and remodelling Ingwall JSCardiovasc Res 2009[Feb]; 81 (3): 412-9Myocytes of the failing heart undergo impressive metabolic remodelling. The time line for changes in the pathways for ATP synthesis in compensated hypertrophy is: flux through the creatine kinase (CK) reaction falls as both creatine concentration ([Cr]) and CK activity fall; increases in [ADP] and [AMP] lead to increases in glucose uptake and utilization; fatty acid oxidation either remains the same or decreases. In uncompensated hypertrophy and in other forms of heart failure, CK flux and fatty acid oxidation are both lower; any increases in glucose uptake and utilization are not sufficient to compensate for overall decreases in the capacity for ATP supply and [ATP] falls. Metabolic remodelling is under transcriptional and post-transcriptional control. The lower metabolic reserve of the failing heart contributes to impaired contractile reserve.|*Energy Metabolism/genetics[MESH]|*Ventricular Remodeling[MESH]|Adenosine Triphosphate/metabolism[MESH]|Adenylate Kinase/metabolism[MESH]|Animals[MESH]|Cardiomyopathy, Hypertrophic, Familial/metabolism/physiopathology[MESH]|Creatine Kinase/metabolism[MESH]|Glycolysis[MESH]|Heart Failure/genetics/*metabolism/physiopathology/therapy[MESH]|Humans[MESH]|Mitochondria, Heart/metabolism[MESH]|Myocardial Contraction[MESH]|Myocardium/enzymology/*metabolism[MESH]|Phenotype[MESH]|Phosphocreatine/metabolism[MESH]|Protein Processing, Post-Translational[MESH]|Time Factors[MESH]|Transcription, Genetic[MESH] |
