The cancer cachexia syndrome, which affects a large proportion of patients with solid tumors, is associated not only with decreasing quality of life but also with a shorter survival time and poor therapy response (1). The imbalance in glycemic homeostasis and the increase of inflammatory response caused by tumoral development are among the main factors involved in the establishment of the cachetic syndrome (1). However, there are no studies that evaluate changes in the endocrine pancreas that may interfere with the imbalance of glycemic control in individuals with cachexia. In previous studies we noted the establishment of cachexia in solid Ehrlich carcinoma bearing-mice. These animals have reduced insulin secretion and decrease in expression of key proteins in insulin signaling pathway, like PKA-α, M3 receptor and AKT. The purpose of this study was to evaluate components of islet inflammatory response of cachetic solid Ehrlich carcinoma bearing-mice that could be involved on decrease in insulin secretion. For this, 40 male adult Swiss mice were divided in two groups. The first group was subcutaneously inoculated with solid Ehrlich tumor (SET) and sacrificed 14 after tumor implantation whilst control group received saline alone (CTL). Real time PCR was performed in islets to evaluate gene expression of toll-like receptors 3, 4, and 9, and Western blotting for determination of proinflammatory cytokines expression such as TNF-α,IL-1β, IFN-α, IFN-γ, IL-6 and IL-8 (replicated 3 times). Western blotting was expressed in arbitrary units and real time PCR was expressed as % of cicles.The results were expressed as Media±SE. Significance of the differences was evaluated by t test followed by Tukey’s test. The significance level was P<0.05. The results revealed that tumor bearing-mice showed a marked increase in islets protein expression of all proinflammatory cytokines analyzed when compared with CTL group (IFN-α – CTL: 3749.7±628.5 vs. SET: 6752.2±672.0; IFN-γ – CTL: 5427.5±219.2 vs. SET: 7699±371.0; IL-6 – CTL: 3332.7±742.9 vs. SET: 7382.2±1239.0; IL-8 – CTL: 4856.2±703.1 vs. SET: 7792.2±661.7; TNF-α – CTL: 5486.6±430.0 vs. SET: 7078±372.9). Further, the results also showed that islets of tumor bearing-mice had increase in gene expression of toll like receptors 3 and 4 but not 9 when compared with CTL group (TLR3 – CTL: 100±1.04 vs. SET :145±1.52; TLR4 – CTL: 100±1.03 vs. SET: 142±1.43). Based on the present data, we can suggest an inflammation status on Islets of Langerhans of SET animals that could be involved in the decrease on insulin secretion previously demonstrated in cachetic tumor-bearing mice.