Influence and related mechanism of Retn gene expression on glucose uptake in 3T3-L1 cells

Influence and related mechanism of Retn gene expression on glucose uptake in 3T3-L1 cells

Abstract

The aim of this article was to investigate the influence and the related mechanism of the Retn gene on glucose uptake and insulin resistance in 3T3-L1 cells. Radioimmunoassay was used to determine glucose uptake in 3T3-L1 cells with different Retn gene expression levels, whether cells were stimulated by insulin or not. RT-PCR and real-time RT-PCR analysis were used to determine the mRNA levels of several glucose transport proteins in 3T3-L1 cells with different Retn gene expression levels, including insulin receptor substrate-1(IRS-1), phosphatidylinositol 3-kinase (PI-3K), AKT-2, glucose transporter-4 (GLUT-4), p38 mitogen-activated protein kinase (p38MAPK) and glycogen synthase kinase-3b (GSK-3β). The glucose uptake decreased with the increase in Retn gene expression in 3T3-L1 cells, which was independent of whether the cells were stimulated by insulin or not. The mRNA expression of two signal proteins PI-3K and AKT-2 decreased and the other two signal proteins, GSK-3β and p38MAPK, increased with Retn overexpression in 3T3-L1 cells. Resistin could induce insulin resistance in adipocytes, which might be related to the changes of some proteins in PI-3K and Ras pathways.