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 Acharya^3,4, Henny H Billett², and Craig A Branch^1,4

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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