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. 2020 Jun 26;41:101045. doi: 10.1016/j.molmet.2020.101045

Figure 2.

Figure 2

Phanginin A inhibits gluconeogenesis by activating SIK1 in primary mouse hepatocytes. (A–B) Primary hepatocytes were incubated with 5 μM phanginin A for different times (A) or with different doses of phanginin A for 2 h (B). SIK1 phosphorylation at Thr182 was detected. met = metformin. (C) Primary hepatocytes were pretreated with or without 0.5 μM of HG-9-91-01 for 30 min and cotreated with 5 μM of phanginin A or 500 μM of metformin for 2 h and then SIK1 phosphorylation was detected. (D) Primary hepatocytes were pretreated with or without 0.5 μM of HG-9-91-01 for 30 min and cotreated with 5 μM or 10 μM of phanginin A or 500 μM of metformin for 4 h and then gluconeogenesis was detected. (E–G) Primary hepatocytes were pretreated with SIK1 siRNA for 48 h followed with or without phanginin A treatment, and the mRNA expression of SIK1-3 (E), SIK1 protein, (F) and gluconeogenesis (G) were detected. (H) The effect of phanginin A on gluconeogenesis in SIK1-knockdown hepatocytes under 10 nM glucagon-induced conditions. All of the results are presented as the mean ± SEM (n = 5 for all of the groups, except for n = 4 in Figure H). ∗P < 0.05 and ∗∗P < 0.01 vs basal controls. ##P < 0.01 vs HG-9-91-01 controls or controls under glucagon-induced conditions.