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Roux-en-Y胃轉(zhuǎn)流術(shù)后肥胖大鼠胰島β細(xì)胞增生及其機(jī)制研究

發(fā)布時(shí)間:2018-04-08 18:26

  本文選題:肥胖 切入點(diǎn):糖尿病 出處:《重慶醫(yī)科大學(xué)》2017年碩士論文


【摘要】:目的:探討Roux-en-Y胃轉(zhuǎn)流術(shù)(Roux-en-Y gastric bypass,RYGB)后肥胖大鼠胰島β細(xì)胞質(zhì)量的改變及其機(jī)制,初步明確RYGB改善肥胖大鼠糖代謝的可能機(jī)制,為臨床上通過RYGB治療肥胖伴糖尿病患者提供理論依據(jù)。方法:(1)SD大鼠共46只,隨機(jī)選取其中40只,高脂飼料喂養(yǎng),建立肥胖大鼠模型,其余6只大鼠,給予普通低脂飼料,作為正常對(duì)照組(NCD組,n=6)。各大鼠單籠飼養(yǎng)共16周,并于每周同一時(shí)間測(cè)量體重。(2)16周末成功誘導(dǎo)22只大鼠肥胖,隨后將大鼠隨機(jī)分為:肥胖組(HFD組,n=6)、RYGB手術(shù)組(RYGB組,n=10)、假手術(shù)組(SHAM組,n=6)。手術(shù)前后分別記錄大鼠體重。(3)術(shù)后6周末行葡萄糖耐量實(shí)驗(yàn),ELISA測(cè)定空腹及餐后30min血清胰島素和C肽水平,并同時(shí)計(jì)算HOME-IR。(4)術(shù)后8周末DEXA測(cè)定大鼠體脂率,收取大鼠附睪脂肪和胰腺組織并稱重,ELISA測(cè)定空腹血清GLP-1水平,大鼠胰腺組織行胰島素免疫組化染色,觀察胰腺形態(tài)學(xué)改變。胰島素免疫熒光染色評(píng)估β細(xì)胞質(zhì)量改變情況。結(jié)果:(1)每組成功建模6只,16周末HFD組大鼠體重、附睪脂肪質(zhì)量、體脂率較NCD組明顯增加。術(shù)后8周,相較HFD組和SHAM組,RYGB組大鼠體重、附睪脂肪質(zhì)量、體脂率明顯下降(均P0.05)。(2)相較NCD組,HFD組大鼠空腹、餐后血糖,空腹胰島素水平,HOME-IR明顯升高。相較HFD組和SHAM組,RYGB組大鼠空腹、餐后血糖,空腹胰島素水平明顯降低,餐后胰島素、C肽水平明顯升高,HOME-IR明顯下降(均P0.05)。(3)免疫組織化學(xué)染色示NCD組、RYGB組胰島素陽(yáng)性染色分布豐富,胰島面積大,而HFD組、SHAM組胰島素染色陽(yáng)性區(qū)域零星分布。(4)術(shù)后大鼠胰腺質(zhì)量-體質(zhì)量比、胰腺組織中相對(duì)b細(xì)胞面積、b細(xì)胞質(zhì)量、單位面積內(nèi)胰島數(shù)量,RYGB組均較HFD組、SHAM組明顯增加(均P0.05),b細(xì)胞平均面積、平均胰島面積各組間無明顯差異(P(29)0.05)。(5)術(shù)后8周末RYGB組大鼠空腹GLP-1水平明顯高于HFD組和SHAM組(P0.05)。結(jié)論:(1)高脂飲食誘導(dǎo)肥胖,糖代謝受損,并伴有胰島素抵抗。(2)RYGB術(shù)后肥胖大鼠胰島b細(xì)胞增生,細(xì)胞質(zhì)量增加,胰島數(shù)量增多,同時(shí)大鼠糖代謝及胰島功能明顯改善,其機(jī)制可能與血清GLP-1水平升高有關(guān)。
[Abstract]:Objective: to investigate the changes and mechanism of islet 尾 cell quality in obese rats after Roux-en-Y gastric bypass operation (Roux-en-Y gastric BYGB), and to clarify the possible mechanism of RYGB in improving glucose metabolism in obese rats, and to provide a theoretical basis for the clinical treatment of obese rats with diabetes by RYGB.Methods A total of 46 Sprague-Dawley rats were selected randomly, 40 of them were fed with high fat diet to establish the obese rat model. The other 6 rats were fed with normal low-fat diet as the normal control group.The serum insulin and C-peptide levels of fasting and postprandial 30min were measured by Elisa at the end of 6 weeks after operation. The body fat rate of rats was measured by DEXA at the end of 8 weeks after operation.The fat and pancreatic tissues of epididymis of rats were collected and the fasting serum GLP-1 levels were measured by weighing Elisa. The pancreatic tissues of rats were stained with insulin immunohistochemical staining to observe the morphologic changes of pancreas.Insulin immunofluorescence staining was used to evaluate the changes of 尾-cell quality.Results (1) six HFD rats in each group were successfully modeled at the end of 16 weeks. The body weight, mass of epididymal fat and body fat rate of each group were significantly higher than those of NCD group.At 8 weeks after operation, the body weight, mass of epididymis fat and body fat rate of rats in HFD group and SHAM group were significantly lower than those in NCD group (P0.05. 0. 2). The fasting postprandial blood glucose and fasting insulin level were significantly higher than those in NCD group.The area of pancreatic islets was large, but the distribution of insulin staining positive area in HFD group was scattered. 4) the ratio of pancreas mass to body mass and the relative area of b cells in pancreatic tissue were measured after operation.The number of islets per unit area in RYGB group was significantly higher than that in HFD group (P 0.05), and there was no significant difference in mean islet area among groups. The fasting GLP-1 level in RYGB group was significantly higher than that in HFD group and SHAM group at the end of 8 weeks after operation.Conclusion 1) High fat diet induced obesity, impaired glucose metabolism, and accompanied by insulin resistance. RYGB, the pancreatic islet b cells proliferated, cell mass increased, the number of islets increased, and the glucose metabolism and islet function of the obese rats improved significantly.The mechanism may be related to the increase of serum GLP-1 level.
【學(xué)位授予單位】:重慶醫(yī)科大學(xué)
【學(xué)位級(jí)別】:碩士
【學(xué)位授予年份】:2017
【分類號(hào)】:R587.1;R589.2;R656.6

【參考文獻(xiàn)】

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本文編號(hào):1722804


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