Ginsenoside F2 Improves Insulin Resistant in 3T3-L1 Adipocytes via the PI3K/Akt Signaling Pathway
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Abstract:
In this study, the effect of ginsenoside F2 (GF2) on insulin resistance in 3T3-L1 adipocytes and the underlying mechanisms were investigated. After 3T3-L1 preadipocytes were induced to differentiate and mature, they were treated with 1 μmol/L dexamethasone for 48 h to establish an insulin resistance model. The insulin-resistant cells were treated with 10 μmol/L rosiglitazone (positive control) and 25, 50 or 100 μmol/L GF2 for 12 h, and the uptake of 2-NBDG by the cells was determined. After the experiments, real-time quantitative PCR was used to evaluate the relative mRNA expression levels of glucose transporter 4 (GLUT-4) and insulin receptor substrate 1(IRS-1) in each group of cells. The protein expression and phosphorylation level of the PI3K/Akt signaling pathway were also evaluated by western blot. The results showed that compared with the model group, 25, 50, and 100 μmol/L GF2 promoted the uptake of 2-NBDG in insulin-resistant 3T3-L1 adipocytes in a dose-dependent manner (increased by 12.58%, 29.07% and 34.62% respectively; p<0.05). After the 12 h treatment with ginsenoside F2, the relative mRNA expression levels of GLUT-4 and IRS-1 as well as the phosphorylation levels of PI3K and Akt increased remarkably (p<0.01. This research shows that GF2 could activate the PI3K/Akt pathway, and improve glucose metabolism and insulin resistance, through promoting the relative mRNA expressions of GLUT-4 and IRS-1 in insulin-resistant 3T3-L1 adipocytes, and increasing the phosphorylation levels of PI3K and Akt proteins.
