Fig. 5: Hepatic glucagon signaling was suppressed by Activin B.

a–c Blood glucose (a, n = 6 mice per group), hepatic glucagon signaling (b), and cAMP contents (c, the sample size (n) is indicated within the graph) in response to glucagon in mice treated with Ad-LacZ or Ad-INHBB. d–f Blood glucose (d, n = 6 mice per group), hepatic glucagon signaling (e), and cAMP contents (f, the sample size (n) is indicated within the graph) in response to glucagon in Inhbb-Lyve1 KO mice. g, h Plasma glucagon levels in fasted adenovirus treated wild-type mice (g, n = 6 mice per group) or Inhbb-Lyve1 KO mice (h, n = 6 mice per group). i, j Relative expression levels of genes encoding phosphdiesterase four subtypes in liver of mice treated with Ad-LacZ or Ad-INHBB (i, n = 3 mice per group) or Inhbb-Lyve1 KO mice (j, n = 3 mice per group). k–m Changes in hepatic cAMP contents (k, the sample size (n) is indicated within the graph) or blood glucose (l, the sample size (n) is indicated within the graph) in response to glucagon challenge and plasma glucagon levels (m, n = 5 mice per group) in mice treated with Ad-LacZ or Ad-INHBB with or without PDE4 inhibitor (PDE4i). Data were shown as mean ± SEM. Statistical significance was determined by unpaired two-tailed Student’s t-test (a, d, g–j); two-way ANOVA (a, d) or with Šídák’s (c, f), or Tukey’s (k–m) multiple comparison test as compared to the respective control group. *p < 0.05, **p < 0.01, ***p < 0.001. Source data are provided as a Source Data File.