RESUMEN
Objective: To investigate the expression of resistin (Retn) gene in the adipose tissues of obese mouse and its influence on the skeletal muscle glucose uptake, in an effort to understand the correlation between obese, resistin, and insulin resistance. Methods: The obese and insulin resistance model was induced with high-fat diet in C57BL/6J mice. Twenty-two weeks later the Lee's index (BMI) and the concentrations of blood glucose and plasma insulin were determined. Glucose tolerance test was carried out to verify the appearance of insulin resistance and the impair to glucose tolerance, with normal mice taken as control. Retn mRNA expression in the adipose tissues of model mice (n=10) and control mice (n=5) was detected by Real-time RT-PCR. The resultant resistin protein was co-cultured with mouse skeletal muscle to assess its influence on glucose uptake. Results: An obese and insulin resistance mouse model was successfully induced with high fat diet. The Retn gene expression in adipose tissues was significantly higher in the obese mice than that in normal control mice (P<0.01). The resultant resistin protein had a significant inhibitory effect on the glucose uptake by skeletal muscle with or without insulin (P<0. 05). Conclusion: It is suggested that the overexpression of Retn gene might be one of the reasons responsible for the decrease of glucose uptake by skeletal muscle and the subsequent insulin resistance in the diet-induced obese mice.
RESUMEN
Objective: To investigate the influence of high expression of Retn gene on glucose uptake by 3T3-L1 cells and to study its mechanism in inducing insulin resistance. Methods: (1) Radioimmunoassay was used to determine the glucose uptake by 3T3-L1 cells with low-, normal- and high-level Retn expression under basal and insulin-stimulated states. (2) RT-PCR and real-time RT-PCR were used to determine the mRNA levels of several glucose transport proteins in 3T3-L1 cells with different expression of Retn, 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-3β(GSK-3β). Results: The uptake of glucose decreased with the increase of Retn expression under basal and insulin-stimulated conditions. The mRNA expression of 2 signal protein PI-3K and AKT-2 decreased with the increase of Retn expression; and the expression of GSK-3β and p38MAPK increased with the increase of Retn expression. Conclusion: Resistin protein can induce insulin resistance in adipocytes, which might be related to the expression changes of some proteins in PI-3K and Ras pathways.