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. 2009 Apr 15;23(8):975–985. doi: 10.1101/gad.1742509

Figure 6.

Figure 6.

Germline deletion of Cdkn2a rescues glucose metabolism and β-cell proliferation defects in βEzh2KO mice. (A) Fasting blood glucose in male triple knockout mice lacking Ezh2 in β cells and Ink4a/Arf (designated as βEzh2KO; Cdkn2a−/−), and βEzh2KO and littermate control Ezh2f/f mice tested at 1 mo. n = 6–11 for each group. (B) Glucose tolerance testing. (C) Area under curve (AUC) from B. (D) Plasma insulin levels at the indicated times following glucose injections assessed in 1-mo-old mice after overnight fasting. n = 5–6 for each group. (E–G) Total pancreas insulin content (E), pancreatic β-cell mass (F), and quantification of BrdU+ insulin+ cells as a percentage of all insulin+ cells (G) in male triple knockout βEzh2KO; Cdkn2a−/− mice, and βEzh2KO and littermate control Ezh2f/f mice at 1 mo. n = 3–4 mice for each group. A, F, and G are box-whisker plots. (*) P < 0.05, (**) P < 0.01, (***) P < 0.001. (NS) Not significant.