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This astrocyteneuron lactate shuttle (ANLS), initially hypothesized by Pellerin and Magistretti, holds that BBB cells take up blood glucose via astrocytic/endothelial GLUT1 transport, allowing cerebral lactate buffering by astrocytic glycogen stores [56]

This suggests that the temporal relationships of KEAP1 disruption and LCS3 treatment may also be a factor, with simultaneous suppression of KEAP1 and treatment with LCS3 having detrimental effects on cell viability