牙周炎与牙周治疗对肥胖大鼠胰岛素抵抗作用的影响

A preliminary study of mechanism of periodontitis and periodontal therapy influence in insulin resistance for obesity rats

目的:探索实验性牙周炎和基础牙周治疗,可能影响肥胖合并牙周炎大鼠胰岛素抵抗的机制。方法:采集前期建模成功的肥胖组,肥胖合并牙周炎组,牙周炎治疗组以及空白对照组大鼠的血液及器官标本,测量身体指数,与胰岛素抵抗相关数据及观察病理学改变。结果:4组比较:牙周炎合并肥胖症时,出现了较单纯肥胖更加严重的胰岛素抵抗和胰岛结构功能的破坏。经牙周治疗后,炎症状态及胰岛素抵抗出现了好转的趋势。病理学标本也提示了这一结果。结论:合并牙周炎会加重肥胖的炎症状态,加重胰岛素抵抗。通过进行基础的牙周治疗可以缓解炎症,改善胰岛素抵抗的情况。IRS-1、IRS-2介导的信号通路受阻,以及PDX-1、GK、GLUT等蛋白表达受抑制,可能与肥胖及肥胖合并牙周炎引起的胰岛素抵抗相关。

Objective To explore the mechanism of the experimental periodontitis and initial periodontal therapy on insulin resistance of obese rats associated with periodontitis. Methods Blood samples were collected from SD rats of obese group, periodontitis associated with obese group, periodontal therapy group and control group. Body index, data about insulin resistance and Observed pathological changes were calculated. Results Comparison of four groups： more severe insulin resistance and islet structural dysfunction was observed in obesity with periodontitis group than that of group with obesity alone. After periodontal therapy, inflammation and insulin resistance may be improved. Results from pathological specimens also supported this result. Conclusions The periodontitis with obesity can enhance the inflammatory state of obesity and cause the deterioration of insulin resistance. The initial periodontal treatment can relieve the inflammation of obesity with periodontitis and improve the resistance of insulin. It may be the reason of insulin resistance when obesity with periodontitis that the signaling pathways of IRS-1 and IRS-2 blocked, and PDX-1, GK, GLUT and other protein expression inhibited.