Apical periodontitis (AP) and smoking may be associated with metabolic syndrome, diabetes mellitus and insulin resistance (IR). Melatonin (MEL) is a hormone with antioxidant, anti-inflammatory properties and participation in bone remodeling. Previous studies show that MEL improves insulin sensitivity and insulin signaling in skeletal muscle of rats with AP. It is known that inflammatory processes in different regions of the human body can promote IR. In this context, we hypothesized that the metabolic alterations in rats with AP are more pronounced with passive tobacco inhalation and the administration of MEL may prevent or decrease IR. The objective of this work will be to evaluate insulin sensitivity and characterize the histopathological inflammation of the heart, trachea, lung and liver of adult rats with AP submitted to passive tobacco inhalation treated with MEL. Will be used 80 Wistar rats with 60 days of age distributed in 8 groups: control (CN); smoking rats (T); rats with AP (AP); smoking rats with AP (T+AP); control using MEL (ME); smoking rats using MEL (T+ME); rats with AP using MEL (AP+ME); smoking rats with AP using MEL (T+AP+ME). The smokers groups will receive passive cigarette inhalation for 50 days, and on the 20th day, the AP groups will be submitted to the induction of apical periodontitis, with the aid of a carbon steel drill in the upper and lower first and second molars on the right side. Furthermore, the animals in the ME groups will be treated with melatonin (5 mg/Kg, orally by gavage) from the 20th to the 50th experimental day. At the end of the treatment, the following will be analyzed: 1) histology of the lung, heart, trachea and liver; 2) glycemia, insulinemia and insulin sensitivity (HOMA-IR). Data normality will be evaluated by the Shapiro-Wilk test. Depending on the results of the normality test, parametric or non-parametric tests will be used to compare glycemia, insulinemia, insulin sensitivity and histopathological analysis between groups. The significance level will be 5%.
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