تغییر بیان ژن SHIP2 (SH2 domain containing inositol 5-phosphatase) با استفاده از سیستم رتروویروس در سلول های کبدی HepG2

Introduction: Dyslypydmy is one of the risk factors of cardiovascular disease in diabetics. Dyslypydmy is diagnosed by increasing in plasma triglyceride density, decreasing HDL Cholesterol, and increasing LDL especially small LDL. Several evidences from human and animal studies indicate that the role of insulin resistance is a major cause of hypertrigly ceridemia in diabetics and people with metabolic syndrome, respectively. Hepatic lipogenesis and the production of rich lipoproteins from triglyceride are set by the inositol phosphatidylinositol kinase (PI3K). However, the negative regulator of route SHIP2 is not well defined in this process (hepatic lipogenesis). Materials and Methods: In this study, the gene expression SHIP2 has been modified by the retroviruses system and the function of intracellular insulin signaling has been studied. Findings: The results show that increasing in expression SHIP2 is lead to decreasing in AKT phosphorylation as one of the mediators of insulin signaling in addition, reducing performance of SHIP2 increase the AKT phosphorylation and improves the intracellular insulin signaling in the liver cells Hep G2. Discussion and Conclusion: Based on the key role AKT phosphorylation in glucose metabolism and lipid, cell models produced can be used in the studies of metabolism of lipids and lipoproteins.