Fig. 1

P301S mice show neither peripheral nor brain insulin resistance. a Intraperitoneal glucose tolerance test (IPGTT) in 5 month old WT non-transgenic and P301S transgenic mice. At time 0, P = 0.9; 15 min, P = 0.29; 30 min, P = 0.33; 60 min, P = 0.3; 120 min, P = 0.26; two-way ANOVA followed by Holm-Sidak multiple comparison test. P301S, n = 10; WT, n = 12. b IPGTT AUC. P = 0.17; Student t-test. c Insulin tolerance test (ITT) in 5 month old WT non-transgenic and P301S transgenic mice. At time 0, P = 0.09; 15 min, P = 0.95, 30 min, P = 0.69; 45 min, P = 0.73; 60 min, P = 0.24; 90 min, P = 0.11; 120 min, P = 0.22; two-way ANOVA followed by Holm-Sidak multiple comparison test. P301S, n = 12; WT, n = 6. In a and c, data points represent the average glycemia ± SEM. d ITT AUC. P = 0.50, Student t-test. e-f Glucose concentration (e) and insulin levels (f) in the cortex of 5-month old P301S and WT mice. n = 6 / group. Glucose and insulin concentrations were normalized to the sample protein content. Bars represent the average ± SEM. In panel e, P = 0.79; panel f, P = 0.24; Student t-test. g Western blot of mTOR, IRβ and Akt and total tau in the cortex. Actin and Tubulin were analyzed as a loading control. h Quantitative analysis of protein expression of IRβ (WT, n = 9; P301S, n = 12), AKT (WT, n = 8; P301S, n = 12) and mTOR (WT, n = 6; P301S, n = 7) in the cortex of 5-month old P301S and WT mice. Protein levels were normalized to actin. Data are expressed as percentage of WT. Bars represent the average ± SEM. IRβ, P = 0.06; AKT, P = 0.09; mTOR, P = 0.14; Student t-test