Abstract #2612

Anaplerotic Flux Into Citric Acid Cycle 4-Carbon Intermediates is Phenotypically Increased in a Murine Model of Heart Failure

Aslan Turer¹, Thomas Gillette¹, Shawn Burgess², Craig Malloy², and Matthew Merritt³

¹Cardiology, UT Southwestern Medical Center, Dallas, TX, United States, ²AIRC, UT Southwestern Medical Center, Dallas, TX, United States, ³Biochemistry and Molecular Biology, University of Florida, Gainesville, FL, United States

Heart failure (HF) was studied using a murine model of aortic constriction. Hearts were perfused to steady state using [1,6-¹³C₂]glucose, [1,3-¹³C₂]acetoacetate, and [U-¹³C]fatty acids. Substrate selection for acetyl-CoA production was measured using isotopomer analysis by carbon-13 NMR. A standard model which includes oxidative flux as well as pyruvate anaplerosis (Y_PC) via pyruvate carboxylase or the malic enzyme was evaluated. Inconsistencies in the fits led to proposal of a more complicated model that also includes anaplerosis through the succinyl-CoA pathway (Y_s), leading to significantly better fits. We hypothesize that induction of the Y_s anaplerotic pathway is phenotypic of HF.

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