【摘要】：一、研究背景和目的胃腸道是人體重要的內(nèi)分泌器官,胃腸功能對(duì)于血糖的調(diào)控具有重要意義。一方面,高血糖可以影響胃腸動(dòng)力,引起惡心、嘔吐、腹痛、飽脹等不適癥狀,影響血糖控制;另一方面,胃腸動(dòng)力的改變影響營(yíng)養(yǎng)物質(zhì)吸收和胃腸激素分泌也會(huì)引起血糖變化。所以調(diào)節(jié)胃腸動(dòng)力的治療手段可以用來(lái)干預(yù)高血糖。胃腸肌電活動(dòng)與胃腸動(dòng)力密切相關(guān)。目前已知高血糖可以引起胃電節(jié)律紊亂。然而,小腸肌電活動(dòng)測(cè)量困難,是否高血糖可引起小腸電節(jié)律紊亂的研究極少。自主神經(jīng)功能障礙也是糖尿病患者的重要并發(fā)癥,但它在高血糖誘導(dǎo)的腸電節(jié)律紊亂中的作用尚不知曉。因此,本研究探索了高血糖對(duì)于小腸肌電活動(dòng)的影響和機(jī)制,以及自主神經(jīng)在其中的作用。前期研究:在肥胖動(dòng)物模型中發(fā)現(xiàn),腸電刺激(IES)可影響胃腸動(dòng)力、胃腸激素的分泌、營(yíng)養(yǎng)物質(zhì)的吸收、從而減輕體重,有望成為2型糖尿病患者的新治療手段之一。本研究(1)在2型糖尿病動(dòng)物模型中,探索了IES對(duì)于血糖的急性及慢性作用;(2)從胃腸動(dòng)力、胃腸激素、食欲、體重、胰島功能等方面探討了IES發(fā)揮降糖作用的可能機(jī)制。二、方法1、高血糖誘導(dǎo)小腸電節(jié)律紊亂伴自主神經(jīng)功能失調(diào)(1)實(shí)驗(yàn)動(dòng)物:雄性自發(fā)性糖尿病Goto-Kakizaki(GK)大鼠和對(duì)照Wistar Kyoto(WKY)大鼠;所有大鼠在試驗(yàn)前接受十二指腸電極埋置手術(shù)和胸部皮下心電圖電極埋置手術(shù)。(2)記錄小腸肌電活動(dòng)和心電圖。(1)頻譜分析小腸肌電活動(dòng)和心電信號(hào)。主要參數(shù)包括:慢波的主要頻率(DF),主功率(DP),正常小腸慢波頻率百分比(%of NSW),每分鐘快波鋒電位數(shù)量。(2)同時(shí)分析心電圖中心率變異(HRV),提取低頻(LF)和高頻(HF)信號(hào),計(jì)算LF/HF比值評(píng)估自主神經(jīng)功能。(3)測(cè)定糖基化血紅蛋白水平(Hb A1c)以及口服葡萄糖耐量試驗(yàn)(OGTT)中不同時(shí)間點(diǎn)的血糖。計(jì)算血糖曲線(xiàn)下面積(AUC)。(4)另一組WKY大鼠給予注射胰高血糖素、模擬高血糖狀態(tài),觀(guān)察血糖變化和小腸電節(jié)律、心臟自主神經(jīng)功能的改變。(5)分析血糖水平和小腸慢波節(jié)律規(guī)整性的相關(guān)性。2、小腸電刺激對(duì)2型糖尿病大鼠血糖調(diào)節(jié)的急性作用及機(jī)制(1)實(shí)驗(yàn)動(dòng)物:20只雄性GK大鼠、10只WKY大鼠,試驗(yàn)前均接受十二指腸電極埋置手術(shù),電極導(dǎo)線(xiàn)自大鼠頸背部皮下穿出,外接刺激器。(2)分組:選擇兩組刺激參數(shù)與無(wú)刺激狀態(tài)(Sham組)比較降糖效果。參數(shù)1組:波寬3ms,波幅2mA,脈沖0.6s on,0.9s off,頻率40Hz,該參數(shù)被認(rèn)為可以改變胃腸動(dòng)力。參數(shù)2組:波寬0.3ms,其余與參數(shù)1相同,該參數(shù)被認(rèn)為可以提高自主神經(jīng)活性。另有Sham組作對(duì)照。選擇兩組IES中最有效的參數(shù)進(jìn)行下面的研究。(3)OGTT,測(cè)定0,15,30,60,120,180min血糖,觀(guān)察急性IES降糖效果。同時(shí)尾靜脈采血ELISA法測(cè)定0,30,60,120min血胰島素、胰高血糖素樣肽1(GLP-1)水平。(4)胰島素耐量試驗(yàn)(ITT),測(cè)定0,30,60,120min血糖,觀(guān)察急性IES對(duì)胰島素敏感性的影響。(5)急性IES聯(lián)合GLP-1拮抗劑使用,觀(guān)察OGTT中血糖變化,探索GLP-1在急性IES中作用。(6)急性IES對(duì)固體胃排空及小腸轉(zhuǎn)運(yùn)的影響。3、小腸電刺激對(duì)2型糖尿病大鼠血糖調(diào)節(jié)的慢性作用及機(jī)制(1)實(shí)驗(yàn)動(dòng)物:20只雄性GK大鼠和10只WKY大鼠,試驗(yàn)前均在十二指腸慢性埋置一對(duì)電極,電極導(dǎo)線(xiàn)通過(guò)外接tether系統(tǒng),連接于刺激器。(2)分組:GK鼠隨機(jī)分為IES組和Sham組:(1)IES組接受持續(xù)8周每夜12h連續(xù)刺激(0.6s on,0.9s off,40Hz,3ms,2m A)。(2)Sham組和WKY組不刺激作對(duì)照。比較IES與Sham組差異。(3)BioDAQ進(jìn)食監(jiān)測(cè)系統(tǒng)連續(xù)自動(dòng)監(jiān)測(cè)記錄大鼠每日進(jìn)食狀況。(4)每周監(jiān)測(cè)體重、空腹血糖(FBG)變化。(5)基線(xiàn)、4周、8周進(jìn)行OGTT,比較IES和Sham組血糖差異。(6)基線(xiàn)、8周檢測(cè)HbA1c、ITT,(7)第8周OGTT同步采血測(cè)定胰島素、GLP-1水平。(8)慢性IES對(duì)胰腺重量,胰島形態(tài)、β細(xì)胞數(shù)量的影響。三、結(jié)果1、高血糖誘導(dǎo)小腸電節(jié)律紊亂伴自主神經(jīng)功能失調(diào)(1)糖尿病大鼠OGTT:血糖及AUC明顯高于正常大鼠。(2)糖尿病大鼠空腹和餐后小腸電節(jié)律的規(guī)律性減低(P0.001)。(3)糖尿病大鼠迷走神經(jīng)活性減低,交感迷走神經(jīng)平衡指數(shù)升高(P0.05)。(4)糖尿病和正常大鼠小腸慢波規(guī)律性與HbA1c水平負(fù)相關(guān)(r=-0.663,P=0.000)。(5)注射胰高血糖素誘導(dǎo)的正常大鼠暫時(shí)性血糖升高,導(dǎo)致小腸慢波紊亂,小腸動(dòng)力減低。(6)注射胰高血糖素后,正常大鼠迷走活性減低,交感迷走神經(jīng)平衡指數(shù)升高。(7)注射胰高血糖素后,血糖的升高與小腸慢波規(guī)律性負(fù)相關(guān)(r=-0.739,P=0.015)。2、小腸電刺激對(duì)2型糖尿病大鼠血糖調(diào)節(jié)的急性作用及機(jī)制(1)與Sham組相比:(1)IES-3ms組明顯降低OGTT前30min血糖(P0.001)。(2)60min~120min,IES-3ms和IES-0.3ms均降低血糖16-20%(P0.05)。(3)兩參數(shù)組OGTT血糖AUC無(wú)差異。(2)ITT血糖水平:IES-3ms和Sham組無(wú)差異,即IES未改變胰島素敏感性。(3)GLP-1拮抗劑阻斷了IES 30~60min的降糖效果(P0.05)。(4)IES提高了糖負(fù)荷后30min GLP-1分泌和胰島素分泌(P0.05)。(5)急性IES-3ms,加快了小腸轉(zhuǎn)運(yùn)(P=0.004),但是沒(méi)有改變胃排空。(三)小腸電刺激對(duì)2型糖尿病大鼠血糖調(diào)節(jié)的慢性作用及機(jī)制(1)糖負(fù)荷后血糖:(1)治療4周末,IES僅降低30min血糖(P0.05)。(2)治療8周末,IES明顯降低15min-120min血糖20-30%(15min和30min P0.02,60min,90min和120min P0.01)。(3)IES組0min血糖下降13%(P0.02),OGTT血糖AUC減少22%(P=0.002)。(2)IES降低空腹血糖10%-15%(第6周末P0.05,第8周末P0.01,第7周末P=0.07)。(3)IES減輕體重:慢性IES在第8周減重10%(P0.05),但是對(duì)食欲沒(méi)有明顯影響(P0.05)。(4)HbA1c:IES明顯降低HbA1c水平6%(P0.05),HbA1c的改變與體重減低無(wú)關(guān)(R~2=0.153,P0.05)。(5)血GLP-1和胰島素水平:8周治療末,IES組空腹和OGTT 30min,GLP-1水平明顯高于Sham組。IES提高了30min血胰島素水平(P0.05),但是沒(méi)有改變胰島素曲線(xiàn)下面積(P0.05)。(6)胰腺重量:Sham組體重標(biāo)化的胰腺重量明顯低于WKY組(P0.05)。而IES組胰腺重量與WKY組無(wú)差異。(7)胰島的形態(tài)和功能:在一定范圍內(nèi),慢性IES可提高胰島β細(xì)胞數(shù)量,恢復(fù)胰島的形態(tài)和結(jié)構(gòu),調(diào)節(jié)α和β細(xì)胞比例。四、結(jié)論1、自發(fā)性高血糖和胰高血糖素誘導(dǎo)的高血糖狀態(tài),均導(dǎo)致小腸肌電活動(dòng)障礙。自主神經(jīng)功能損害可能參與了高糖誘導(dǎo)的小腸電節(jié)律紊亂。2、急性IES:可降低2型糖尿病大鼠糖負(fù)荷后血糖。其降糖作用可能通過(guò)GLP-1介導(dǎo)。胃腸動(dòng)力和自主神經(jīng)調(diào)控均參與了IES的作用。3、慢性IES:可降低餐后及空腹血糖,其降糖作用可能通過(guò)調(diào)控GLP-1分泌、改善胰島β細(xì)胞功能實(shí)現(xiàn)。
[Abstract]:First, research background and objective gastrointestinal tract is an important endocrine organ of the human body. Gastrointestinal function is of great significance for the regulation of blood sugar. On the one hand, high blood sugar can affect gastrointestinal motility, cause nausea, vomiting, abdominal pain, fullness and other discomfort symptoms, affect blood sugar control; on the other hand, gastrointestinal motility changes affect nutrient absorption and gastrointestinal Hormone secretion can also cause blood sugar changes. So the treatment of gastrointestinal motility can be used to interfere with hyperglycemia. The gastrointestinal myoelectric activity is closely related to gastrointestinal motility. At present, hyperglycemia can cause gastroelectric disorder. However, the measurement of small intestinal myoelectric activity is difficult, and whether hyperglycemia can cause the study of intestinal rhythmic disorders is the most important. Less. Autonomic nervous dysfunction is also an important complication of diabetic patients, but its role in hyperglycemic induced intestinal dysrhythmicity is not yet known. Therefore, this study explored the effects and mechanisms of hyperglycemia on small intestinal myoelectric activity, as well as the use of autonomic nerves in the intestinal electromyography. Electrical stimulation (IES) can affect gastrointestinal motility, secretion of gastrointestinal hormones, absorption of nutrients, and loss of weight, which is expected to become one of the new treatments for patients with type 2 diabetes. (1) in the model of type 2 diabetes, the acute and chronic effects of IES on blood glucose are explored; (2) from gastrointestinal motility, gastrointestinal hormones, appetite, body weight, pancreas Island function and other aspects of the possible mechanisms for IES to play a hypoglycemic effect. Two, method 1, hyperglycemia induced small intestinal dysregulation with autonomic dysfunction (1) experimental animals: male spontaneous diabetes Goto-Kakizaki (GK) rats and control Wistar Kyoto (WKY) rats; all rats were treated with duodenal electrode implantation before experiment and Subcutaneous electrocardiogram electrode implantation. (2) recording small intestinal myoelectric activity and electrocardiogram. (1) spectrum analysis of small intestinal myoelectric activity and electrocardiogram. The main parameters include the main frequency of slow wave (DF), the main power (DP), the percentage of normal small intestinal slow wave frequency (%of NSW), the number of fast wave front potential per minute. (2) analysis of the center rate of electrocardiogram at the same time HRV, extracting low frequency (LF) and high frequency (HF) signals and calculating the LF/HF ratio to evaluate autonomic function. (3) determination of glycated hemoglobin level (Hb A1c) and oral glucose tolerance test (OGTT) at different time points. Calculate the area of blood glucose under the blood sugar curve (AUC). (4) another group of WKY rats give injection of glucagon to simulate hyperglycemia Changes in blood sugar and small intestine electric rhythm and changes in autonomic nervous function of the heart. (5) analysis of the correlation between blood glucose level and small intestinal rhythm regulation.2, the acute effect and mechanism of small intestinal electrical stimulation on the regulation of blood glucose in type 2 diabetic rats (1) experimental animals: 20 male rats, 10 WKY rats, and duodenal electricity before the test. Extremely burial operation, the electrode traverse of the rat's neck subcutaneous and external stimulator. (2) group: select two groups of stimulation parameters and no stimulation state (Sham group) to compare the effect of hypoglycemic. Parameters 1 groups: wave width 3MS, amplitude 2mA, pulse 0.6s on, 0.9s off, frequency 40Hz, this parameter is considered to be able to change the gastrointestinal motility. Parameter 2: wave width 0.3ms, and the rest and reference The parameters were 1 the same, and the parameters were considered to be able to improve the autonomic nerve activity. And the Sham group was used as a control. The following study was conducted in the two groups of the most effective parameters. (3) OGTT, 0,15,30,60120180min blood glucose, and acute IES hypoglycemic effect. 0,30,60120min blood insulin, glucagon like peptide 1 (GLP) was measured by the ELISA method in the tail vein. -1) level. (4) insulin tolerance test (ITT), determination of 0,30,60120min blood sugar and the effect of acute IES on insulin sensitivity. (5) acute IES combined with GLP-1 antagonists, observation of blood glucose changes in OGTT, and the role of GLP-1 in acute IES. (6) the effect of acute IES on gastric emptying and small intestinal transport is.3, small intestinal electrical stimulation to type 2 diabetes mellitus The chronic effect and mechanism of blood glucose regulation in rats (1) experimental animals: 20 male GK rats and 10 WKY rats, a pair of electrodes were embedded in the duodenum, and the electrode wire was connected to the stimulator by external tether system. (2) the GK rats were divided into IES and Sham groups randomly: (1) the IES group received continuous 12h continuous stimulation for 8 weeks (0.6s). On, 0.9s off, 40Hz, 3MS, 2m A). (2) the difference between the Sham group and the WKY group was not stimulated. The difference between the IES and Sham group was compared. (3) the BioDAQ eating monitoring system continuously and automatically monitored the daily feeding status of the rats. (4) the body weight and the fasting blood glucose were monitored every week. (5) the baseline, 4 weeks, and 8 weeks of blood glucose differences were compared. (6) baseline and 8 weeks C, ITT, (7) eighth weeks OGTT synchronous blood sampling for insulin, GLP-1 level. (8) the effect of chronic IES on pancreatic weight, islet morphology, and beta cell number. Three, 1, high blood sugar induced intestinal dysregulation with autonomic dysfunction (1) diabetic rats, OGTT: blood glucose and AUC were significantly higher than normal rats. (2) the fasting and postprandial small intestine in diabetic rats The regularity of electrical rhythm decreased (P0.001). (3) the activity of vagus and the sympathetic vagus balance index increased (P0.05) in diabetic rats. (4) the regularity of the slow wave of the small intestine in diabetes and normal rats was negatively correlated with the HbA1c level (r=-0.663, P=0.000). (5) the temporary glucose increased in normal rats induced by glucagon injection, resulting in the slow wave of the small intestine. (6) after injection of glucagon, the normal rat vagus activity decreased and the sympathetic vagus balance index increased. (7) after the injection of glucagon, the increase of blood glucose was negatively correlated with the regularity of the slow wave of the small intestine (r=-0.739, P=0.015).2. The acute effect and mechanism of small bowel electrospiny on the regulation of blood glucose in type 2 diabetic rats (1) and S Group ham compared: (1) group IES-3ms significantly reduced pre OGTT 30min blood sugar (P0.001). (2) 60min~120min, IES-3ms and IES-0.3ms reduced blood sugar 16-20% (P0.05). (3) two ginseng array OGTT glucose AUC was no difference. (2) blood glucose level: neither group nor the difference in insulin sensitivity. (3) antagonist antagonist blocking the effect of hypoglycemic effect (P0.05) (4) IES increased 30min GLP-1 secretion and insulin secretion after sugar load (P0.05). (5) acute IES-3ms, accelerated intestinal transport (P=0.004), but did not change gastric emptying. (three) the chronic effect and mechanism of small intestinal electrical stimulation on the regulation of blood glucose in type 2 diabetic rats (1) glucose after sugar load: (1) the 4 weekend, IES only reduced 30min blood sugar (P) (0.05) (2) for the 8 week of treatment, IES significantly reduced 15min-120min blood glucose 20-30% (15min and 30min P0.02,60min, 90min and 120min P0.01). (3) 0min glucose decreased by 13% (P0.02) and 22% of blood glucose decreased (2). (sixth weekend, eighth weekend, seventh weekend). Weight loss 10% (P0.05), but no significant effect on appetite (P0.05). (4) HbA1c:IES significantly reduced HbA1c level 6% (P0.05), HbA1c changes were not related to weight loss (R~2=0.153, P0.05). (5) blood GLP-1 and insulin levels: 8 weeks of treatment at the end of the treatment, IES group empty and OGTT 30min. But there was no change in the area under the insulin curve (P0.05). (6) pancreas weight: the weight of the pancreas in group Sham was significantly lower than that in group WKY (P0.05). The weight of pancreas in group IES was not different from that in group WKY. (7) the form and function of pancreatic islet: in a certain range, chronic IES could raise the number of islet beta cells, restore the morphology and structure of the islets, and regulate the alpha and beta Cell ratio. Four, conclusion 1, spontaneous hyperglycemia and glucagon induced hyperglycemia all lead to the disturbance of small intestinal myoelectric activity. The impairment of autonomic nervous function may be involved in high glucose induced intestinal dysregulation of.2, and acute IES: can reduce glucose after glucose load in type 2 diabetic rats. Its hypoglycemic effect may be mediated by GLP-1. Both intestinal motility and autonomic nerve regulation are involved in the role of IES in.3. Chronic IES: can reduce postprandial and fasting blood glucose, and its hypoglycemic effect may improve the function of islet beta cells by regulating the secretion of GLP-1.
【學(xué)位授予單位】：南京醫(yī)科大學(xué)
【學(xué)位級(jí)別】：博士
【學(xué)位授予年份】：2015
【分類(lèi)號(hào)】：R587.1

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