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Abstract #2168

Cerebral metabolic and physiological evidence supporting a shift toward glycolysis in a mouse model with congenital anemia.

Min Hui Cui1, Sandra Suzuka2, Mary E Fabry2, Seetharama A Acharya3,4, Henny H Billett2, and Craig A Branch1,4

1Radiology, Albert Einstein College of Medicine, Bronx, NY, United States, 2Medicine/Hematology, Albert Einstein College of Medicine, Bronx, NY, United States, 3Albert Einstein College of Medicine, Bronx, NY, United States, 4Physiology & Biophysics, Albert Einstein College of Medicine, Bronx, NY, United States

The effect of congenital anemic hypoxia on brain energy metabolism was studied on BERK-Hemi mouse exhibiting poor oxygen delivery secondary to reduced hemoglobin oxygen affinity. Regionally increased CBF in BERK-Hemi mouse was correlated with decreased mean diffusivity and tissue T1. Additionally, BERK-Hemi mouse exhibited elevated concentrations in N-acetylaspartate, glutamate, total choline and glucose in thalamus, but a lower concentration of glutamine. Together, the results suggest BERK-Hemi mice develop a compensatory mechanism which leads to increased glycolysis to combat hypoxia and increased reactive oxygen stress.

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