Figure 1.

Activation of the GLP-1R and GIPR within the β cell is required for regulation of glucose by DPP4i

(A–E) Abundance of Gipr and Glp1r mRNA in islets of male and female control and DIRKO^{β-cell−/−} mice normalized to Tbp. (B and C) Expression of Gipr (B) and Glp1r (C) mRNA transcripts in whole extracts of jejunum, epididymal white adipose tissue (eWAT), and lung tissue normalized to Tbp. (D-E) Oral glucose tolerance test (2 g/kg) glycemia (D) and AUC (E) in male and female control (MIP-Cre and Dpp4^fl/fl) mice administered sitagliptin (14 μg/mouse or 10 mg/kg) by oral gavage 30 min prior to gavage of glucose.

(F and G) Oral glucose tolerance test (2 g/kg) glycemia (F) and AUC (G) in DIRKO^{β-cell−/−} mice administered sitagliptin (14 μg/mouse or 10 mg/kg) by oral gavage 30 min prior to gavage of glucose.

(H) Oral glucose tolerance test AUC in male and female control compared to DIRKO^{β-cell−/−} mice without sitagliptin. Statistical differences between groups were analyzed by an unpaired t test (A–C, H) or ANOVA (1 way or mixed-effects analysis) with post-hoc Tukey test (D–G). Data are represented as mean ± SEM, ∗p < 0.05, ∗∗p < 0.01 (control compared to sita 10 mg/kg), ∗∗∗p < 0.001, ∗∗∗∗p < 0.0001.