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. 2018 Apr 16;67(7):1332–1344. doi: 10.2337/db17-1352

Figure 4.

Figure 4

βDoc2b-dTg mice are protected from STZ-induced glucose intolerance, fasting hyperglycemia, and β-cell apoptosis. A: Male βDoc2b-dTg mice aged 12–13 weeks were injected daily on days 1–5 with STZ (35–40 mg/kg body weight), and on day 24 were fasted 6 h and subjected to an IPGTT. AUC quantification for IPGTT; n = 3 βDoc2b-dTg Dox– and n = 5 βDoc2b-dTg Dox+ mice. B: Fasting blood glucose of STZ-treated βDoc2b-dTg mice; n = 3 βDoc2b-dTg Dox– and n = 5 βDoc2b-dTg Dox+ mice. C: Immunofluorescence staining and quantification of TUNEL-positive β-cells (indicated by arrows in images, expressed as % of total β-cells) were conducted on fixed pancreata of βDoc2b-dTg Dox– and βDoc2b-dTg Dox+ mice; n = 3 βDoc2b-dTg Dox– and n = 5 βDoc2b-dTg Dox+. Bar = 20 µm. Islet β-cell area (D) and islet β-cell mass (E) were calculated from fixed βDoc2b-dTg whole pancreata immunostained for insulin content. The dotted line indicates the β-cell area and mass of non–STZ-treated Wt mice in our colony (38); n = 3 mice/group (three sections per mouse). *P < 0.05; **P < 0.01. Data for A are shown as mean ± SEM and for B–E are shown as mean ± SD.