Adrianus J. Bakermans1, Michael S. Dodd2, Klaas Nicolay1, Jeanine J. Prompers1, Sander M. Houten3, Damian J. Tyler2
1Biomedical NMR, Eindhoven University of Technology, Eindhoven, Netherlands; 2Cardiac Metabolism Research Group, University of Oxford, Oxford, United Kingdom; 3Laboratory Genetic Metabolic Diseases, Academic Medical Center, Amsterdam, Netherlands
Glucose oxidation may be unable to compensate sufficiently to maintain myocardial energy homeostasis in patients affected by fatty acid β-oxidation disorders. The flux through the pyruvate dehydrogenase (PDH) complex was studied using hyperpolarized 13C-MRS of [1-13C]pyruvate in the in vivo heart of long-chain acyl-CoA dehydrogenase knock-out (LCAD KO) mice and controls in fed and fasted conditions.
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