Fig. 1

Trex1-deficient rats develop spontaneous diabetes. A Blood glucose levels of WT (n = 32; female, n = 20; male, n = 12) and Trex1^−/− (n = 46; female, n = 26; male, n = 20) rats were measured monthly from 4 weeks postnatal until 48 weeks, and the individual values of blood glucose were plotted versus ages. B Diabetes incidence in WT (n = 32) or Trex1^−/− (n = 46) rats from A. C Percent HbA1c in WT (n = 7) and Trex1^−/− (n = 9) rats, the detected serum from different weeks of age. D The blood glucose changes after challenged with glucose, were measured with time, using WT (n = 10) and Trex1^−/− (n = 10) rats at 12 weeks of age. Glucose was injected intraperitoneally at a dose of 2 g/kg. E Quantification of the area under curve (AUC) in D for the intraperitoneal glucose tolerance test. F Survival curve for WT (n = 32) and Trex1^−/− (n = 46) rats from A. G Blood glucose was measured periodically from WT + STZ group (n = 15) or Trex1^−/−  + STZ group (n = 20) after STZ injection. STZ, streptozotocin, intraperitoneal injection, 30 mg/kg. H Diabetes incidence in WT (n = 15) or Trex1^−/− (n = 20) rats after STZ injection. All data are represented as mean ± SEM; Each dot represents one independent biological replicate; Log-rank (Mantel-Cox) test in B, F, H; Unpaired t test in C; Welch’s t test in E