Figure 6.

i-αOGT^KOmice show trend of reduced α-cell mass, as well as reduced circulating glucagon and impaired PTT. Immunofluorescent staining for glucagon (green) and DAPI (blue) of fixed pancreatic sections at 20× magnification, in male control and i-αOGT^KO mice at 15 weeks post-tamoxifen treatment (scale = 50 μm) (A). Quantification of α-cell mass in male control and i-αOGT^KO mice 15 weeks post-tamoxifen treatment (B), (n = 4 per group). Random fed blood glucose levels in male control and i-αOGT^KO mice 2 months post-tamoxifen treatment (C), (n = 4 per group). Random fed circulating glucagon levels in male control and i-αOGT^KO mice 2 months post-tamoxifen treatment (D), (n = 4 per group). In vitro glucose inhibited glucagon secretion in male mice (E), (n = 3 per group). Glucose levels after intraperitoneal injection of pyruvate in male control and i-αOGT^KO mice 2 months post-tamoxifen treatment (F) (n = 4 per group). Intraperitoneal glucagon challenge in male control and i-αOGT^KO mice 2 months post-tamoxifen treatment (G) (n = 4 per group). Body weight measured in male i-αOGT^KO mice (H) (n = 4 per group) from 0 to 15 weeks or in a different cohort of mice at 24 weeks (I, n = 4) post-tamoxifen treatment. IPGTT done at 24 weeks (J, n = 4) post-tamoxifen treatment. Data represent mean ± SEM, ∗p < 0.05, ∗∗p < 0.01, ∗∗∗p < 0.001 compared with control. Analysis was done by unpaired, two-tailed Student’s t-tests, repeated measures one-way ANOVA, and two-way ANOVA.