In vitro (Bérdad et al., 1997) and in vivo (Carvalho-Filho et al., 2005) studies have shown that cytokines decrease glucose uptake in skeletal muscle in response to insulin by increasing the expression of inducible nitric oxide synthase (iNOS). Thyroid hormone treatment was shown to increase the insulin sensitivity and decrease the glycemic levels in db/db mice (Lin and Sun, 2011). In this context, this study aimed to evaluate whether thyroid hormone treatment could affect insulin sensitivity in diabetic rats by altering TNF-α, IL-6 and/or iNOS expression in oxidative skeletal muscle. Methods: Male Wistar rats were assorted in control (C), diabetic (D) and T3-treated diabetic group (D T1,5) – 15. 10-3 μg. g-1 b.w.. The diabetes was induced by aloxan injection (150 mg. Kg-1 b.w.) and after 15 days, the glycemia was measured. The animals which presented glycemia levels higher than 250 mg/dL were included in the diabetic groups. A subset of diabetic rats was treated with T3 for a 28 day-period (D T1,5). After this period, the skeletal muscle (soleus) was removed and TNF-α, IL-6 and iNOS content was analyzed through western blotting. Results: T3 treatment decreased the amount of TNF-α, IL-6 and iNOS protein and improved insulin sensitivity in oxidative skeletal muscle tissue (soleus), as shown by the increased Akt kinase phosphorilation in response to insulin administration. Conclusion: The present data provide evidence that at least part of the benefits of T3 treatment in insulin sensitivity of diabetic rats occurs by its negative modulation of cytokines and iNOS expression.