Abstract
Background: The aim of this study was to explore the mechanism by which amentoflavone (AME) improves insulin resistance in a human hepatocellular liver carcinoma cell line (HepG2). Methods: A model of insulin resistant cells was established in HepG2 by treatment with high glucose and insulin. The glucose oxidase method was used to detect the glucose consumption in each group. To determine the mechanism by which AME improves insulin resistance in HepG2 cells, enzyme-linked immunosorbent assay (ELISA) and western blotting were used to detect the expression of phosphatidyl inositol 3-kinase (PI3K), Akt, and pAkt; the activity of the enzymes involved in glucose metabolism; and the levels of inflammatory cytokines. Results: Insulin resistance was successfully induced in HepG2 cells. After treatment with AME, the glucose consumption increased significantly in HepG2 cells compared with the model group (MG). The expression of PI3K, Akt, and pAkt and the activity of 6-phosphofructokinas (PFK-1), glucokinase (GCK), and pyruvate kinase (PK) increased, while the activity of glycogen synthase kinase-3 (GSK-3), phosphoenolpyruvate carboxylase kinase (PEPCK), and glucose-6-phosphatase (G-6-Pase) as well as the levels of interleukin-6 (IL-6), interleukin-8 (IL-8), tumor necrosis factor-α (TNF-α), and C reactive protein (CRP) decreased. Conclusions: The mechanism by which treatment with AME improves insulin resistance in HepG2 cells may involve the PI3K-Akt signaling pathway, the processes of glucose oxygenolysis, glycogen synthesis, gluconeogenesis and inflammatory cytokine expression.
Highlights
With the rapid development of the social economy, the incidence of metabolic diseases such as obesity, diabetes, and metabolic syndrome has increased
The glucose consumption was significantly increased in the metformin group (MF) and in the AMEI, AMEII, and AMEIII groups compared with the model group (MG) (p < 0.01 or p < 0.05)
The activities of PFK-1, GCK, and pyruvate kinase (PK) were significantly increased in the MF, AMEI, AMEII, and AMEIII groups compared with the MG (p < 0.01 or p < 0.05)
Summary
With the rapid development of the social economy, the incidence of metabolic diseases such as obesity, diabetes, and metabolic syndrome has increased. Many studies have investigated the pathogenesis of these diseases in which insulin resistance plays an important role [1]. Insulin is the only hypoglycemic hormone in the body. Defects in insulin signal transduction lead to insulin resistance, which is the main cause of metabolic diseases [2,3]. The liver is the main tissue that supplies energy to the body. Insulin resistance in the liver will induce substance and energy dysmetabolism. Liver sensitivity to insulin is important for the stabilization of blood sugar levels. The aim of this study was to explore the mechanism by which amentoflavone (AME) improves insulin resistance in a human hepatocellular liver carcinoma cell line (HepG2)
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