Fig. 4: Activin B suppressed hepatic gluconeogenesis in an insulin-independent manner.
From: Activin B improves glucose metabolism via induction of Fgf21 and hepatic glucagon resistance
a, b Blood glucose (a) and plasma insulin levels (b) of STZ mice treated with Ad-LacZ or Ad-INHBB during GTT. Ad-LacZ; n = 8, Ad-INHBB; n = 7. c Relative expression levels of genes regulating hepatic gluconeogenesis of STZ mice treated with Ad-LacZ or Ad-INHBB. Ad-LacZ; n = 6, Ad-INHBB; n = 4. d PEPCK protein levels in the liver from 4 independent animals. e Blood glucose levels of STZ mice during PTT. n = 5 mice per group. f, g Fasting blood glucose levels (f) or blood glucose levels during PTT (g) in STZ-treated Inhbb-Lyve1 KO or control mice. Inhbb-Flox; n = 6, Inhbb-Lyve1 KO; n = 9. h Glucose production in primary hepatocytes treated with recombinant Activin B. n = 4. i–k Relative expression levels of Pck1 treated with recombinant Activin B with or without Forskolin and Dexamethasone (Frk/Dex) (i, n = 3), subtype-specific ALK inhibitors (j, n = 3), or treated with adenovirus encoding constitutive active mutant of ALK2 (Ad-ALK2(QD)) (k, n = 3). Data were presented as means ± SEM. Statistical significance was determined by unpaired two-tailed Student’s t-test (a, f, g); two-way ANOVA (g) or with Šídák’s (a, c, j), Dunnett’s (e), or Tukey’s (i) multiple comparison test, one-way ANOVA with Dunnett’s (e) or Šídák’s (h, k) multiple comparison test as compared to the respective control group. *p < 0.05, **p < 0.01, ***p < 0.001. #p < 0.05 versus normal mice in (e). Source data are provided as a Source Data File.
