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. 2023 Mar 20;15(6):1490. doi: 10.3390/nu15061490

Figure 1.

Figure 1

Skatole attenuates palmitic acid (PA)-induced hepatic lipid accumulation and lipogenesis-related proteins and restores glucose metabolism and insulin resistance (IR) in HepG2 cells. (A) HepG2 cells were treated with different concentrations of skatole (1–10 μΜ) with 0.25 mM PA for 24 h, and the lipid accumulation was analyzed using Nile Red staining. Scale bar, 25 μM. (B) The relative fluorescence intensity of intrahepatic lipids was analyzed using Columbus software. (C) HepG2 cells were treated with 5 μΜ skatole and 0.25 mM PA for 24 h. Western blot analysis indicated that skatole regulated lipogenesis-related factors. (D) Relative protein expression levels for lipogenesis-related factors. The relative expression levels of fatty acid synthase (FAS) and Lipin-1 were normalized with β-actin. (E) Glucose uptake was evaluated with 2-NBDG fluorescence intensity in HepG2 cells after the same treatment described in (A,B). (F) Western blot analysis indicated that skatole regulated gluconeogenesis-related factors and IR in HepG2 cells after the same treatment described in (C). (G) The relative expression levels of G6pase and PEPCK were normalized with β-actin, and p-AKT was normalized with AKT. All experiments were performed as three independent samples, and the values are shown as mean ± SD, analyzed by one-way ANOVA. (n = 3–5, *** p < 0.001, ** p < 0.01, * p < 0.05, ns: not significant. CTL: control).