Fig. 5.

Impaired insulin signalling may have contributed to reduced APOE-ε4 hiBMEC glycolysis. (a, b) Representative Western blots with quantification of insulin receptor (INSR) in APOE-ε3 and -ε4 hiBMEC (n = 9 samples per genotype). (c, d) Representative Western blots with quantification of p-Akt and Akt in APOE-ε3 and -ε4 hiBMEC treated with 10 μg/mL insulin for 30 min (n = 9 samples per condition). (e, f) Representative Western blots with quantification of membrane and cytosolic GLUT1 in APOE-ε3 and -ε4 hiBMEC (n = 9 samples per genotype). (g, h) Representative Western blots with quantification of membrane GLUT1 in hiBMEC treated with 10 μg/mL insulin and 1 μM Wortmannin for 30 min (n = 9 samples per condition). (i) Seahorse Glycolytic Rate Assay and (j) basal GlycoPER in hiBMEC following treatment with 10 μg/mL and 1 μM Wortmannin for 30 min (n = 10 samples per treatment group). Data were analysed using (b) Mann–Whitney test, (d, f) Two-way ANOVA with Fishers Least Significant Difference Test, and (h, j) Kruskall-Wallis with Dunn's multiple comparison test.