dc.contributorUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-27T11:29:01Z
dc.date.accessioned2022-10-05T18:49:01Z
dc.date.available2014-05-27T11:29:01Z
dc.date.available2022-10-05T18:49:01Z
dc.date.created2014-05-27T11:29:01Z
dc.date.issued2013-05-01
dc.identifierJournal of Endodontics, v. 39, n. 5, p. 648-652, 2013.
dc.identifier0099-2399
dc.identifierhttp://hdl.handle.net/11449/75226
dc.identifier10.1016/j.joen.2012.12.031
dc.identifierWOS:000319031900014
dc.identifier2-s2.0-84876666173
dc.identifier9235743081667362
dc.identifier4408095517346846
dc.identifier8275401688702343
dc.identifier0000-0003-4859-0583
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/3924164
dc.description.abstractIntroduction: Inflammatory cytokines are associated with decreased insulin signal transduction. Moreover, local oral inflammation, such as that accompanying periodontal disease, is associated with insulin resistance and type 2 diabetes mellitus. The aim of this study was to evaluate the effect of periapical lesions (PLs) on insulin signaling and insulin sensitivity in rats. We hypothesized that PLs alter systemic insulin signaling and insulin sensitivity via elevated plasmatic tumor necrosis factor α (TNF-α). Methods: Wistar rats were divided into control (CN) and PL groups. PLs were induced by exposing pulpal tissue to the oral environment. After 30 days, insulin sensitivity was measured using the insulin tolerance test. After euthanization, maxillae were processed for histopathology. Plasmatic concentrations of tumor necrosis factor α (TNF-α) were determined via the enzyme-linked immunosorbent assay. Insulin signal transduction was evaluated using insulin receptor substrate tyrosine phosphorylation status and serine phosphorylation status in periepididymal white adipose tissue via Western blotting. For insulin signaling and insulin tolerance tests, the analyses performed were analysis of variance followed by the Tukey post hoc test. For TNF-α analysis, the Student's t test was used. In all tests, P <.05 was considered significant. Results: The rats with PLs showed higher plasmatic TNF-α, lower constant rate for glucose disappearance values, and reduced pp185 tyrosine phosphorylation status but no change in serine phosphorylation status in white adipose tissue after insulin stimulation. Conclusions: PLs can cause alterations to both insulin signaling and insulin sensitivity, probably because of elevation of plasmatic TNF-α. The results from this study emphasize the importance of the prevention of local inflammatory diseases, such as PLs, with regard to the prevention of insulin resistance. Copyright © 2013 American Association of Endodontists.
dc.languageeng
dc.relationJournal of Endodontics
dc.relation2.886
dc.relation1,585
dc.rightsAcesso restrito
dc.sourceScopus
dc.subjectDiabetes mellitus
dc.subjectinsulin resistance
dc.subjectperiapical lesions
dc.subjecttumor necrosis factor α
dc.titlePeriapical lesions decrease insulin signal and cause insulin resistance
dc.typeArtigo


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