本文選題：飲食誘導(dǎo) + 肥胖��； 參考：《南方醫(yī)科大學》2017年博士論文

【摘要】：第一章飲食誘導(dǎo)肥胖復(fù)合牙周炎大鼠模型的建立目的建立肥胖復(fù)合牙周炎大鼠模型方法雄性Sprague-Dawley(SD)大鼠,4周齡,隨機分為普通飼料組和高脂飼料組。連續(xù)喂養(yǎng)16周,篩選肥胖大鼠30只。隨機分為肥胖對照組(10只)和肥胖復(fù)合牙周炎組(簡稱復(fù)合組,20只)。20周齡時,復(fù)合組大鼠雙側(cè)上頜第二磨牙用3-0慕絲線進行牙周結(jié)扎,誘導(dǎo)實驗性牙周炎。結(jié)果(1)喂養(yǎng)至20周齡,高脂飼料組的體重顯著高于普通飼料組(體重大于對照組15%)。(2)病理檢查發(fā)現(xiàn),復(fù)合組牙齦上皮屏障出現(xiàn)糜爛性破壞,結(jié)合上皮向根方增殖,牙周袋形成,牙槽骨喪失,肥胖復(fù)合牙周炎大鼠模型成功。結(jié)論高脂飲食喂養(yǎng)16周可建立肥胖大鼠模型;肥胖大鼠模型基礎(chǔ)上進行牙周絲線結(jié)扎,可建立肥胖復(fù)合牙周炎大鼠模型。第二章實驗性牙周炎對肥胖大鼠血清C-反應(yīng)蛋白(C-reactive protein,CRP)及胰島素抵抗的影響目的探討實驗性牙周炎對肥胖大鼠血清CRP及胰島素抵抗隨時間的變化。方法復(fù)合組及肥胖組在牙周結(jié)扎前、結(jié)扎后1周、4周眼底眶靜脈采血2mL行空腹血糖、胰島素以及糖化血紅蛋白(HbAlc)的測定,計算胰島素抵抗指數(shù)(HOMA-IR),胰島β細胞功能指數(shù)(HOMA-β);ELISA檢測血清CRP。結(jié)果(1)牙周結(jié)扎后4周,復(fù)合組大鼠的HOMA-IR(30.29±4.77)顯著高于對照組(21.95±2.97);復(fù)合組大鼠HOMA-β(755.36±98.11)顯著低于肥胖對照組(913.53±94.50)。(2)牙周結(jié)扎后1周,復(fù)合大鼠的CRP水平(203.78±53.71ng/mL)顯著高于肥胖組(156.37±33.84ng/mL)。結(jié)論(1)實驗性牙周炎加重肥胖大鼠的胰島素抵抗狀態(tài),下調(diào)β細胞功能。(2)實驗性牙周炎影響大鼠血清CRP水平。第三章非手術(shù)牙周治療對肥胖大鼠血清炎癥因子及胰島素抵抗的影響目的探討非手術(shù)牙周治療對肥胖大鼠代謝指標及炎癥因子的影響。方法復(fù)合組大鼠16只,按體重排序,依次分為兩組,治療組(8只):拆除絲線,牙周沖洗;未治療組(8只):不予拆除牙周絲線。2周后行口服葡萄糖耐量試驗(OGTT),眼底眶靜脈采血2mL行空腹血糖、胰島素以及HbA1c的測定,計算 HOMA-IR,HOMA-β;ELISA 檢測血清 CRP。結(jié)果(1)治療組空腹血糖(5.06±0.69mmol/L)低于未治療組(5.61±0.19mmol/L),HOMA-β(974.54±419.37)高于未治療組(645.37±73.47)。(2)治療組 CRP(140.99±32.10ng/mL)低于未治療組(173.43±28.54ng/mL)(3)OGTT中,治療組在60min、120min的血糖值低于未治療組,糖面積(9.62±0.57)低于治療組未治療組(12.59±0.58)。結(jié)論非手術(shù)牙周治療下調(diào)大鼠血清CRP水平,改善胰島β細胞功能,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 鹵4.77 in the compound group was significantly higher than that in the control group (21.95 鹵2.97), and the HOMA- 尾 -nmL level in the compound group was significantly lower than that in the obese control group (913.53 鹵94.50 ng 路mL-1). The CRP level in the compound group was 203.78 鹵53.71 ngmL) significantly higher than that in the obese group (156.37 鹵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 鹵0.69 mmol / L) lower than that in the untreated group (5.61 鹵0.19 mmol / L), and the glucose area was 9.62 鹵0.57) significantly lower than that in the untreated group (645.37 鹵73.47 mg 路L / L). The CRP(140.99 鹵32.10 ng / mL in the treatment group was lower than that in the untreated group (173.43 鹵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 鹵0.57) lower than that in the untreated group (12.59 鹵0.58). Conclusion Non-operative periodontal therapy can down-regulate serum CRP level, improve islet 尾 cell function and improve glucose tolerance in rats.
【學位授予單位】：南方醫(yī)科大學
【學位級別】：博士
【學位授予年份】：2017
【分類號】：R781.42;R589.2;R-332

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