Fig. 3.

d-Allulose improves glucose tolerance via GLP-1R signaling. Allu at 1 g kg⁻¹ was p.o. administered at 60 min prior to ipGTT (2 g kg⁻¹), a–g, insulin tolerance test (ITT, 1 IU kg⁻¹, h–k) and pyruvate tolerance test (PTT, 2 g kg⁻¹, l-o). Ex(9-39) at 200 nmol kg⁻¹ was i.p. injected at 75 min prior to ipGTT (e, f), ITT (i, j), and PTT (m, n). a–d Effect of p.o. Allu on blood glucose and plasma insulin levels in ipGTT in C57BL/6J mice fasted overnight (16 h, a, b) and for 4 h (c, d). n = 5. e, f Ex(9-39) treatment blunted the action of Allu to attenuate rises of blood glucose (e) and its area under the curve (AUC, f) in ipGTT in C57BL/6J mice fasted 4 h. n = 7–8. g p.o. Allu failed to improve glucose tolerance in Glp1r KO mice fasted for 4 h (n = 6). h–k Allu potentiated insulin action to lower blood glucose (h) and its AUC (j) in ITT, and these effects were abolished in the presence of Ex(9-39) in C57BL/6J mice fasted 4 h (i, j) and in Glp1r KO mice (k). n = 5–11. l–o Allu suppressed blood glucose elevation (l) and its AUC (n) in PTT, and these effects were completely blocked in the presence of Ex(9-39) in C57BL/6J mice fasted overnight (m, n) and in Glp1r KO mice fasted overnight (o). n = 5–6. Different letters indicate p < 0.05 by two-way ANOVA followed by Tukey’s test (e), and *p < 0.05, **p < 0.01 by two-way ANOVA followed by Bonferroni’s test vs. saline group (a–c, h, l). In d, #p < 0.05 by repeated measures ANOVA followed by Dunnett’s test vs. 0 min in Allu group. In f, j, n, different letters indicate p < 0.05 by one-way ANOVA followed by Tukey’s test. Error bars are SEM