Resumo (EN)
Objective – To evaluate the effect of periodontal disease in insulin sensitivity in the modulation of proteins of the insulin signaling pathway such as IR, IRS-1, IRS-2, Akt, ERK and activation of the JNK and IKK in liver and muscle of rats. Methods – In this study, we evaluated the regulation of insulin signaling, JNK and IKK activation and IRS-1ser307 phophorylation by immunoprecipitation and immunoblotting in the liver and muscle of rats with periodontitis induced by ligature for 28 days. Results – Chronic inflammatory periodontal disease (periodontitis) leads to gingival inflammation, destruction of periodontal tissues and loss of alveolar bone. Periodontitis increased blood glicose and plasma insulin levels during the oGTT, and reduced the glicose disappearance rate in the insulin tolerance test, characterized a state of insulin resistance. In periodontitis rats we observed a reduction in insulin-induced IR, IRS-1, IRS-2, Akt phosphorylation in liver and muscle, compared to controls. JNK and IKK activity and IRS-1ser307 phosphorylation were higher in the tissues of rats with periodontitis. Conclusions – In summary, the insulin resistance, induced by periodontitis, is accompanied by activation of the JNK and IKK pathways and IRS-1ser307 phosphorylation. The impairment of the insulin signaling in these tissues may lead to insulin resistance in periodontitis.