Effect and mechanism of Vaspin on insulin resistance of 3T3-L1 adipocytes induced by palmitic acid

Objective To investigate the effects of vaspin on insulin resistants of 3T3-L1 adipocyte through the insulin receptor substrates (IRS)/phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/glucose transporter (Glut) signaling pathway. Methods 3T3-L1 cells cultured by palmitic acid (PA) were used to establish insulin resistance models, which were divided into PA group, PA+ 100 ng/ml vaspin group, PA+ 200 ng/ml vaspin group, PA+ 400 ng/ml vaspin group and PA+ 400 ng/ml vaspin+ wortmannin (PI3K inhibitor) group. Glucose uptake and consumption were assessed by 2-deoxy H3-D-glucose incorporation and glucose oxidase-peroxidase respectively. IRS/PI3K/Akt/Glut signaling pathway was evaluated using reverse transcription polymerase chain reaction and Western blot analysis. Results Compared with PA group, glucose uptake and consumption increased gradually with the increasing of vaspin concentration in other groups (P<0.05). mRNA levels of IRS-1, Akt and Glut 4 increased gradually as vaspin concentration increasing (P<0.05), and the ratios of p-IRS-1 to IRS-1, p-Akt to Akt and Glut 4 protein level also showed the same trends (P<0.05). However, glucose uptake and consumption in PA+ 400 ng/ml vaspin+ wortmannin group were less than that of PA+ 400 ng/ml vaspin group (P<0.05). PA+ 400 ng/ml vaspin+ wortmannin group showed lower mRNA and protein phosphorylation levels of IRS-1, Akt and Glut 4 (P<0.05), and that the ratios of p-IRS-1 to IRS-1, p-Akt to Akt and Glut 4 protein levels decreased (P<0.05). Conclusions Vaspin can improve the insulin sensitivity of 3T3-L1 adipocyte by activating IRS/PI3K/Akt/Glut signaling pathway. Key words: Vaspin; Insulin resistance; 3T3-L1 adipocyte; IRS/PI3K/Akt/Glut