实验性牙周炎及非手术牙周治疗对肥胖大鼠血清炎症因子和胰岛素抵抗影响的研究

发布时间：2018-04-23 10:27

本文选题：饮食诱导 + 肥胖　；参考：《南方医科大学》2017年博士论文

【摘要】：第一章饮食诱导肥胖复合牙周炎大鼠模型的建立目的建立肥胖复合牙周炎大鼠模型方法雄性Sprague-Dawley(SD)大鼠,4周龄,随机分为普通饲料组和高脂饲料组。连续喂养16周,筛选肥胖大鼠30只。随机分为肥胖对照组(10只)和肥胖复合牙周炎组(简称复合组,20只)。20周龄时,复合组大鼠双侧上颌第二磨牙用3-0慕丝线进行牙周结扎,诱导实验性牙周炎。结果(1)喂养至20周龄,高脂饲料组的体重显著高于普通饲料组(体重大于对照组15%)。(2)病理检查发现,复合组牙龈上皮屏障出现糜烂性破坏,结合上皮向根方增殖,牙周袋形成,牙槽骨丧失,肥胖复合牙周炎大鼠模型成功。结论高脂饮食喂养16周可建立肥胖大鼠模型;肥胖大鼠模型基础上进行牙周丝线结扎,可建立肥胖复合牙周炎大鼠模型。第二章实验性牙周炎对肥胖大鼠血清C-反应蛋白(C-reactive protein,CRP)及胰岛素抵抗的影响目的探讨实验性牙周炎对肥胖大鼠血清CRP及胰岛素抵抗随时间的变化。方法复合组及肥胖组在牙周结扎前、结扎后1周、4周眼底眶静脉采血2mL行空腹血糖、胰岛素以及糖化血红蛋白(HbAlc)的测定,计算胰岛素抵抗指数(HOMA-IR),胰岛β细胞功能指数(HOMA-β);ELISA检测血清CRP。结果(1)牙周结扎后4周,复合组大鼠的HOMA-IR(30.29±4.77)显著高于对照组(21.95±2.97);复合组大鼠HOMA-β(755.36±98.11)显著低于肥胖对照组(913.53±94.50)。(2)牙周结扎后1周,复合大鼠的CRP水平(203.78±53.71ng/mL)显著高于肥胖组(156.37±33.84ng/mL)。结论(1)实验性牙周炎加重肥胖大鼠的胰岛素抵抗状态,下调β细胞功能。(2)实验性牙周炎影响大鼠血清CRP水平。第三章非手术牙周治疗对肥胖大鼠血清炎症因子及胰岛素抵抗的影响目的探讨非手术牙周治疗对肥胖大鼠代谢指标及炎症因子的影响。方法复合组大鼠16只,按体重排序,依次分为两组,治疗组(8只):拆除丝线,牙周冲洗;未治疗组(8只):不予拆除牙周丝线。2周后行口服葡萄糖耐量试验(OGTT),眼底眶静脉采血2mL行空腹血糖、胰岛素以及HbA1c的测定,计算 HOMA-IR,HOMA-β;ELISA 检测血清 CRP。结果(1)治疗组空腹血糖(5.06±0.69mmol/L)低于未治疗组(5.61±0.19mmol/L),HOMA-β(974.54±419.37)高于未治疗组(645.37±73.47)。(2)治疗组 CRP(140.99±32.10ng/mL)低于未治疗组(173.43±28.54ng/mL)(3)OGTT中,治疗组在60min、120min的血糖值低于未治疗组,糖面积(9.62±0.57)低于治疗组未治疗组(12.59±0.58)。结论非手术牙周治疗下调大鼠血清CRP水平,改善胰岛β细胞功能,改善糖耐量。
[Abstract]:Chapter 1 Establishment of Diet-Induced Rats with Obesity and periodontitis objective to establish a rat model of obesity combined periodontitis methods male Sprague-Dawley SD rats were randomly divided into normal diet group and high-fat diet group. Thirty obese rats were selected by continuous feeding for 16 weeks. The rats were randomly divided into obese control group (n = 10) and obese combined periodontitis group (n = 20). At the age of 20 weeks, bilateral maxillary second molars were ligated with 3-0 filaments to induce experimental periodontitis. Results 1) when fed to the age of 20 weeks, the body weight of the high-fat diet group was significantly higher than that of the normal diet group (body weight was higher than that of the control group). Pathological examination showed that the gingival epithelial barrier appeared erosive destruction in the compound group, the epithelium of the composite group proliferated to the root side, and the periodontal bag formed. Alveolar bone loss, obesity and periodontitis rat model was successful. Conclusion Obesity rat model can be established by high-fat diet feeding for 16 weeks, and obesity combined periodontitis rat model can be established by ligation of periodontal filaments on the basis of obese rat model. Chapter 2 effects of experimental periodontitis on serum C-reactive protein (CRP) and insulin resistance in obese rats objective to investigate the changes of serum CRP and insulin resistance in obese rats with experimental periodontitis. Methods 2mL was collected from orbital vein before periodontal ligation and 1 week after ligation in compound group and obesity group. Fasting blood glucose, insulin and HbAlc were measured. Insulin resistance index (HOMA-IRN) and islet 尾 cell function index (尾 -HOMA- 尾) were calculated. Serum CRP was detected by Elisa. Results at 4 weeks after periodontal ligation, the HOMA-IR(30.29 卤4.77 in the compound group was significantly higher than that in the control group (21.95 卤2.97), and the HOMA- 尾 -nmL level in the compound group was significantly lower than that in the obese control group (913.53 卤94.50 ng 路mL-1). The CRP level in the compound group was 203.78 卤53.71 ngmL) significantly higher than that in the obese group (156.37 卤84ngmL / mL) 1 week after periodontal ligation. Conclusion (1) Experimental periodontitis exacerbates insulin resistance and down-regulates 尾 -cell function in obese rats.) Experimental periodontitis affects serum CRP level in rats. Chapter 3 effects of nonoperative periodontal therapy on serum inflammatory factors and insulin resistance in obese rats objective to investigate the effects of nonoperative periodontal therapy on metabolic indexes and inflammatory factors in obese rats. Methods Sixteen rats in the compound group were divided into two groups according to their body weight. Eight rats in the treatment group were divided into two groups: removal of filaments and periodontal irrigation; In the untreated group, 8 rats were treated with oral glucose tolerance test (OGTT) after 2 weeks without removal of periodontal filaments, fasting blood glucose, insulin and HbA1c were measured by 2mL collected from orbital veins. Serum CRPs were measured by HOMA-IRMA-HOMA- 尾 -ELISA. Results 1) the fasting blood glucose in the treatment group was 5.06 卤0.69 mmol / L) lower than that in the untreated group (5.61 卤0.19 mmol / L), and the glucose area was 9.62 卤0.57) significantly lower than that in the untreated group (645.37 卤73.47 mg 路L / L). The CRP(140.99 卤32.10 ng / mL in the treatment group was lower than that in the untreated group (173.43 卤28.54ng/mL)(3)OGTT). The blood glucose level in the treatment group was lower than that in the untreated group at 60 min, and the glucose area was 9.62 卤0.57) lower than that in the untreated group (12.59 卤0.58). Conclusion Non-operative periodontal therapy can down-regulate serum CRP level, improve islet 尾 cell function and improve glucose tolerance in rats.
【学位授予单位】：南方医科大学
【学位级别】：博士
【学位授予年份】：2017
【分类号】：R781.42;R589.2;R-332

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