摘要：

Elevated,levels ,of resistin ,have ,been ,proposed ,to cause ,insulin resistance ,and therefore, may serve as a link between obesity and type 2 diabetes. However, its role in skeletal muscle metabolism is unknown. In this study, we examined the effect of resistin oninsulin-stimulated ,glucose ,uptake ,as well ,as the ,upstream ,insulin signaling components,in L6 rat skeletal muscle,cells that were,either incubated,with recombinant resistin or stably ,transfected ,with a vector ,containing ,the myc-tagged ,mouse ,resistin gene. Transfected ,clones ,expressed ,intracellular resistin which ,was ,released ,in the medium.,Incubation with recombinant,resistin resulted in a,dose-dependent,inhibition of insulin-stimulated 2-deoxyglucose (2-DOG) uptake. The inhibitory effect of resistin ,on insulin-stimulated 2-DOG uptake ,was ,not due ,to impaired ,Glut-4 translocation ,to the plasma membrane. Furthermore, resistin did not alter the IR content and its phosphorylation, nor did it affect insulin-stimulated IRS-1 tyrosine phosphorylation, its

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