Effects of periodontitis on onset and severity of insulin resistance

Objectives: The objective of this study was to determine the causal effect of periodontitis ± dietary fat on onset of insulin resistance and T2DM using a rat model system that simulates obesity in humans.

Methods: A total of 28, 5-week old female Zucker diabetic fatty rats (ZDF, fa/fa) were divided into four groups with periodontitis induced by ligature in one-half of the animals. The four groups of 7 animals included: high fat-fed periodontitis (HF/P), high fat-fed no periodontitis (HF/C), low fat-fed periodontitis (LF/P), and low fat-fed no periodontitis (LF/C) rats. Fasting plasma insulin and glucose levels were measured every week for 13 weeks to determine onset of insulin resistance (IR) by HOMA. Glucose tolerance tests were performed in weeks 1, 4, 8, 10 and 12 to assess onset of T2DM. The serum levels of TNFα, leptin, triglyceride, and free fatty acid were also determined at week 13 at which time the animals were sacrificed.

Results: HF/P rats developed severe IR compared to HF/C rats in week 6 and 7 (p <0.01). The onset of severe IR as indicated by HOMA was approximately 3 weeks earlier in HF/P rats versus HF/C rats. Severe glucose intolerance was evident in week 10 in HF/P and 12 in HF/C rats. There was no difference in the severity and onset of IR between LF/P and LF/C rats. IR was less in LF versus HF fed rats (p < 0.0001). The serum level of TNFα was significantly higher in HF/P versus HF/C rats in samples collected at 13 weeks (p <0.01). The levels of leptin, free fatty acid, and triglycerides were not significantly different between the four groups.

Conclusion: Periodontitis in conjunction with a high fat diet accelerates the onset of IR and appears to accelerate the onset of severe glucose intolerance and thus T2DM.