Disruption of Growth Factor Receptor–Binding Protein 10 in the Pancreas Enhances β-Cell Proliferation and Protects Mice From Streptozotocin-Induced β-Cell Apoptosis

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FIG. 5.
FIG. 5.

Pancreatic-specific knockout of Grb10 enhances resistance to STZ-induced diabetes in mice. Male pGrb10KO and WT control mice (2 months old) were treated with STZ (75 mg/kg) for 5 days. Blood glucose levels (A) and body weight (B) were measured in WT (n = 8) and pGrb10KO (n = 11) mice every 3 days at the same time point (12 p.m. each day) after STZ treatment. Data are shown as mean ± SEM. *P < 0.05; **P < 0.01; ***P < 0.001 (one-way repeated-measure ANOVA). C: pGrb10KO (n = 6) and WT (n = 8) mice were treated with STZ for 22 days and killed. Pancreases were isolated and weighed. D: pGrb10KO mice (n = 4) and WT littermates (n = 3) were treated with STZ for 22 days and then killed. Serum was collected for insulin measurement. E: Average β-cell mass between pGrb10KO (n = 4) and WT littermates (n = 3). F: Cell apoptosis rate was analyzed by TUNEL assay between pGrb10KO mice (n = 4) and WT littermates (n = 3). Mice were injected with STZ twice daily (0 and 24 h) and killed 24 h later. More than 2,500 insulin-positive cells were counted per mice. Black bars, Grb10 flox+/−; white bars, pGrb10 KO. Data are shown as mean ± SEM. *P < 0.05; **P < 0.01 (t test).

This Article

  1. Diabetes vol. 61 no. 12 3189-3198