Fig. 4: GLUT1 cKO astrocytes have enhanced glucose metabolism.
From: Astrocytic GLUT1 deletion in adult mice enhances glucose metabolism and resilience to stroke
a Representative glucose sensor traces showing the astrocytic glucose level increase in response to transient elevation of [Glc]O from 5 mM to 25 mM in Ctrl and cKO brain slices. b Glucose rise rate (dashed lines in (a)) was similar between Ctrl (n = 53 cells from 9 slices, 5 animals) and cKO (n = 88 cells from 12 slices, 6 animals, p = 0.967, two-sided linear mixed model). c Glucose increase (Δ[Glc]) was significantly higher in cKO astrocytes (n = 88 cells from 12 slices, 6 animals) compared to Ctrl (n = 53 cells from 9 slices, 5 animals, p < 0.0001, two-sided linear mixed model). d Schematic of glucose consumption assay: Glucose uptake was inhibited with the GLUT blocker cytochalasin B (CytoB) to assess glucose consumption rate in astrocytes. Glc-6P, glucose-6-phosphate. e Representative traces showing the astrocytic glucose decline in Ctrl and cKO brain slices during CytoB incubation. f Glucose consumption rate, measured as the decline in [Glc] (dashed lines in (e)), was 2.6-fold higher in cKO astrocytes (−0.079 ± 0.003 min⁻¹, n = 101 cells from 12 slices, 6 animals) compared to Ctrl (n = 63 cells from 9 slices, 5 animals, −0.030 ± 0.003 min⁻¹, p = 0.002, two-sided linear mixed model). Box plots show the median (center line), quartiles (box bounds), mean (+) and min-to-max (whiskers). Source data are provided as a Source Data file.
