Periodontitis contributes to adipose tissue inflammation through the NF- B, JNK and ERK pathways to promote insulin resistance in a rat model

Abstract This study aimed to investigate the mechanism by which periodontitisaffects the inflammatory response and systemic insulin resistancein the white adipose and liver tissues in an obese rat model. The obese model was generated by feeding rats a high fat diet. The periodontitismodel was induced by ligaturesand injection of “ red complex”, which consisted of Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia, for two weeks. When compared with rats without periodontitis, fasting glucose levels and homeostasis model assessment index were significantly increased in rats with periodontitis, suggesting that periodontitispromotes the development of insulin resistancein obese rats. Gene and protein expression analysis in white adipose and liver tissue revealed that experimental periodontitisstimulated the expression of inflammatory cytokines, such as tumor necrosis factors-alpha, interleukin-1 beta, toll-like receptor2 and toll-like receptor4. Signals associated with inflammation and insulin resistance, including nuclear factor- B, c-Jun amino-terminal kinase and extracellular-signal regulated kinasewere significantly activated in the white adipose tissuefrom obese rats with periodontitiscompared to obese rats without periodontitis. Taken together, these findings suggest that periodontitisplays an important role in aggravating the development of local white adipose inflammation and systemic insulin resistancein rat models.