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. 2015 Nov 30;112(50):15498–15503. doi: 10.1073/pnas.1513872112

Fig. 5.

Fig. 5.

Angptl4 is required for hyperglucagonemia and compensatory α-cell proliferation following GRA treatment. (A and B) C57BL/6J (control) and angptl4−/− mice display a similar α- to β-cell ratio (A) and α-cell density (B). (C) Percentage of Ki67-positive α- and β-cells in young angptl4−/− mice treated for 7 d with PBS (control), GRA, GRA+hAngptl4, or the Pparγ agonist Rosiglitiazone. P = 0.01 (Kruskal–Wallis); adjusted Mann–Whitney P values are 0.02, 0.01, and 0.02 between GRA-, control, and Rosiglitazone-treated vs. GRA+hAngptl4, respectively. (D) Plasma glucagon levels following a 6-h fast in angptl4−/− mice following treatment with PBS, GRA, or GRA+hAngptl4. (E) Fasting glucose levels in 14-wk-old DIO C57BL/6J mice, DIO angptl4−/− mice treated with PBS, or DIO angptl4−/− mice treated with GRA for 7 d. P = 0.03 and P = 0.005 (ANOVA, n = 4–5 per group). (F–H) Percentage of Ki67-positive α- and β-cells (F), α-cell density (G), and 6-h fasting plasma glucagon levels (H) in mice treated as in E. *P < 0.05; **P < 0.01.