Prediabetes Enhances Periodontal Inflammation Consistent With Activation of TLR Mediated NF-кB Pathway in Rats

Methods: In this study, we established prediabetes rat model by feeding high fat diet (HFD). High fat diet induced prediabetic rats (N=7) and normal chow feed rats (N=7) were studied. The animal model was characterized in terms of body weight (BW), the glycemic and insulinemic profiles. The following parameters were assessed to evaluate possible early periodontal alterations and underlying mechanisms: histology analysis of periodontal tissue, as well as the serum and mRNA levels and/or the tissue protein expression of TLRs, myeloid differentiation factor 88 (MyD88), TNF receptor associated factor 6 (TRAF6), NF-кB, cytokines, advanced glucose ends (AGEs) and free fatty acids (FFAs). Results: Prediabetic rats presented higher expression of TLR2 and TLR4 in periodontal tissue in the HFD group compared with the control group, respectively. The TLR2 and TLR4 was mostly expressed in gingiva, in addition to, TLR4 was expressed in periodontal ligament in rats. Furthermore, the MyD88 and TRAF6 protein levels were significantly increased in gingiva in prediabetic rats compared to normal rats. The activity of NF-кB signals was higher in prediabetic rats than in normal rats. Regarding cytokines expression, the TNF-alpha (TNF-α) protein levels and IL-1betta (IL-1β) mRNA levels were significantly increased in the HFD group compared with the control group. In the serum, AGEs levels were significantly increased in the prediabetic rats. Mean FFAs concentrationswere increased in prediabetic rats, compared to normal rats; however, it did not reach statistical significance.