W Zhao1, S-P Zhao. 1. Department of Cardiology, The Second Xiangya Hospital, Central South University, Changsha, Hunan, China. zhshuip@163.com.
Abstract
OBJECTIVE: We aimed to evaluate the effect of atorvastatin on apolipoprotein AV (ApoAV) in HepG2 cells of insulin resistance (IR), and further explore its mechanism. MATERIALS AND METHODS: Firstly, a model of IR in HepG2 cells was established by insulin, and then treated with various concentrations of atorvastatin (0, 10, 100 and 500 nM) for 12 h and 24 h, respectively. Detection of glucose concentration was performed by Glucose Oxidase kit. Subsequently, Enzyme-linked immunosorbent assay (ELISA) kits were used to measure the concentrations of triglyceride (TG), high density lipoprotein (HDL), low density lipoprotein (LDL) and very low density lipoprotein (VLDL). The mRNA levels of ApoAV and ApoAV-related genes, including glucose transporter 1 (Glut1), Glut2, peroxisome proliferator activated receptor α (PPARα), and liver X receptor α (LXRα) were detected by qRT-PCR. RESULTS: We successfully established IR model in HepG2 cells by 10-6 nM insulin. Subsequently, we found that the glucose extraction rate and mRNA level of ApoAV significantly reduced in HepG2 cells of IR (p < 0.05); however, atorvastatin increased the glucose extraction rate and ApoAV mRNA level. Furthermore, atorvastatin inhibited the concentration of TG in HepG2 cells of IR (p < 0.05); however, atorvastatin had no effect on HDL, LDL and VLDL. Also, atorvastatin could increase the mRNA levels of Glut2 but not Glut1, PPARα, and LXRα. CONCLUSIONS: Our study indicated that atorvastatin might inhibit IR induced by insulin through the TG-lowering role of ApoAV. Furthermore, Glut2 might be involved in the effect of atorvastatin on ApoAV in HepG2 cells of IR.
OBJECTIVE: We aimed to evaluate the effect of atorvastatin on apolipoprotein AV (ApoAV) in HepG2 cells of insulin resistance (IR), and further explore its mechanism. MATERIALS AND METHODS: Firstly, a model of IR in HepG2 cells was established by insulin, and then treated with various concentrations of atorvastatin (0, 10, 100 and 500 nM) for 12 h and 24 h, respectively. Detection of glucose concentration was performed by Glucose Oxidase kit. Subsequently, Enzyme-linked immunosorbent assay (ELISA) kits were used to measure the concentrations of triglyceride (TG), high density lipoprotein (HDL), low density lipoprotein (LDL) and very low density lipoprotein (VLDL). The mRNA levels of ApoAV and ApoAV-related genes, including glucose transporter 1 (Glut1), Glut2, peroxisome proliferator activated receptor α (PPARα), and liver X receptor α (LXRα) were detected by qRT-PCR. RESULTS: We successfully established IR model in HepG2 cells by 10-6 nM insulin. Subsequently, we found that the glucose extraction rate and mRNA level of ApoAV significantly reduced in HepG2 cells of IR (p < 0.05); however, atorvastatin increased the glucose extraction rate and ApoAV mRNA level. Furthermore, atorvastatin inhibited the concentration of TG in HepG2 cells of IR (p < 0.05); however, atorvastatin had no effect on HDL, LDL and VLDL. Also, atorvastatin could increase the mRNA levels of Glut2 but not Glut1, PPARα, and LXRα. CONCLUSIONS: Our study indicated that atorvastatin might inhibit IR induced by insulin through the TG-lowering role of ApoAV. Furthermore, Glut2 might be involved in the effect of atorvastatin on ApoAV in HepG2 cells of IR.