高血糖导致小肠电节律紊乱及小肠电刺激对2型糖尿病血糖调控的研究
发布时间：2018-08-07 08:19
【摘要】：一、研究背景和目的胃肠道是人体重要的内分泌器官,胃肠功能对于血糖的调控具有重要意义。一方面,高血糖可以影响胃肠动力,引起恶心、呕吐、腹痛、饱胀等不适症状,影响血糖控制;另一方面,胃肠动力的改变影响营养物质吸收和胃肠激素分泌也会引起血糖变化。所以调节胃肠动力的治疗手段可以用来干预高血糖。胃肠肌电活动与胃肠动力密切相关。目前已知高血糖可以引起胃电节律紊乱。然而,小肠肌电活动测量困难,是否高血糖可引起小肠电节律紊乱的研究极少。自主神经功能障碍也是糖尿病患者的重要并发症,但它在高血糖诱导的肠电节律紊乱中的作用尚不知晓。因此,本研究探索了高血糖对于小肠肌电活动的影响和机制,以及自主神经在其中的作用。前期研究:在肥胖动物模型中发现,肠电刺激(IES)可影响胃肠动力、胃肠激素的分泌、营养物质的吸收、从而减轻体重,有望成为2型糖尿病患者的新治疗手段之一。本研究(1)在2型糖尿病动物模型中,探索了IES对于血糖的急性及慢性作用;(2)从胃肠动力、胃肠激素、食欲、体重、胰岛功能等方面探讨了IES发挥降糖作用的可能机制。二、方法1、高血糖诱导小肠电节律紊乱伴自主神经功能失调(1)实验动物:雄性自发性糖尿病Goto-Kakizaki(GK)大鼠和对照Wistar Kyoto(WKY)大鼠;所有大鼠在试验前接受十二指肠电极埋置手术和胸部皮下心电图电极埋置手术。(2)记录小肠肌电活动和心电图。(1)频谱分析小肠肌电活动和心电信号。主要参数包括:慢波的主要频率(DF),主功率(DP),正常小肠慢波频率百分比(%of NSW),每分钟快波锋电位数量。(2)同时分析心电图中心率变异(HRV),提取低频(LF)和高频(HF)信号,计算LF/HF比值评估自主神经功能。(3)测定糖基化血红蛋白水平(Hb A1c)以及口服葡萄糖耐量试验(OGTT)中不同时间点的血糖。计算血糖曲线下面积(AUC)。(4)另一组WKY大鼠给予注射胰高血糖素、模拟高血糖状态,观察血糖变化和小肠电节律、心脏自主神经功能的改变。(5)分析血糖水平和小肠慢波节律规整性的相关性。2、小肠电刺激对2型糖尿病大鼠血糖调节的急性作用及机制(1)实验动物:20只雄性GK大鼠、10只WKY大鼠,试验前均接受十二指肠电极埋置手术,电极导线自大鼠颈背部皮下穿出,外接刺激器。(2)分组:选择两组刺激参数与无刺激状态(Sham组)比较降糖效果。参数1组:波宽3ms,波幅2mA,脉冲0.6s on,0.9s off,频率40Hz,该参数被认为可以改变胃肠动力。参数2组:波宽0.3ms,其余与参数1相同,该参数被认为可以提高自主神经活性。另有Sham组作对照。选择两组IES中最有效的参数进行下面的研究。(3)OGTT,测定0,15,30,60,120,180min血糖,观察急性IES降糖效果。同时尾静脉采血ELISA法测定0,30,60,120min血胰岛素、胰高血糖素样肽1(GLP-1)水平。(4)胰岛素耐量试验(ITT),测定0,30,60,120min血糖,观察急性IES对胰岛素敏感性的影响。(5)急性IES联合GLP-1拮抗剂使用,观察OGTT中血糖变化,探索GLP-1在急性IES中作用。(6)急性IES对固体胃排空及小肠转运的影响。3、小肠电刺激对2型糖尿病大鼠血糖调节的慢性作用及机制(1)实验动物:20只雄性GK大鼠和10只WKY大鼠,试验前均在十二指肠慢性埋置一对电极,电极导线通过外接tether系统,连接于刺激器。(2)分组:GK鼠随机分为IES组和Sham组:(1)IES组接受持续8周每夜12h连续刺激(0.6s on,0.9s off,40Hz,3ms,2m A)。(2)Sham组和WKY组不刺激作对照。比较IES与Sham组差异。(3)BioDAQ进食监测系统连续自动监测记录大鼠每日进食状况。(4)每周监测体重、空腹血糖(FBG)变化。(5)基线、4周、8周进行OGTT,比较IES和Sham组血糖差异。(6)基线、8周检测HbA1c、ITT,(7)第8周OGTT同步采血测定胰岛素、GLP-1水平。(8)慢性IES对胰腺重量,胰岛形态、β细胞数量的影响。三、结果1、高血糖诱导小肠电节律紊乱伴自主神经功能失调(1)糖尿病大鼠OGTT:血糖及AUC明显高于正常大鼠。(2)糖尿病大鼠空腹和餐后小肠电节律的规律性减低(P0.001)。(3)糖尿病大鼠迷走神经活性减低,交感迷走神经平衡指数升高(P0.05)。(4)糖尿病和正常大鼠小肠慢波规律性与HbA1c水平负相关(r=-0.663,P=0.000)。(5)注射胰高血糖素诱导的正常大鼠暂时性血糖升高,导致小肠慢波紊乱,小肠动力减低。(6)注射胰高血糖素后,正常大鼠迷走活性减低,交感迷走神经平衡指数升高。(7)注射胰高血糖素后,血糖的升高与小肠慢波规律性负相关(r=-0.739,P=0.015)。2、小肠电刺激对2型糖尿病大鼠血糖调节的急性作用及机制(1)与Sham组相比:(1)IES-3ms组明显降低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)两参数组OGTT血糖AUC无差异。(2)ITT血糖水平:IES-3ms和Sham组无差异,即IES未改变胰岛素敏感性。(3)GLP-1拮抗剂阻断了IES 30~60min的降糖效果(P0.05)。(4)IES提高了糖负荷后30min GLP-1分泌和胰岛素分泌(P0.05)。(5)急性IES-3ms,加快了小肠转运(P=0.004),但是没有改变胃排空。(三)小肠电刺激对2型糖尿病大鼠血糖调节的慢性作用及机制(1)糖负荷后血糖:(1)治疗4周末,IES仅降低30min血糖(P0.05)。(2)治疗8周末,IES明显降低15min-120min血糖20-30%(15min和30min P0.02,60min,90min和120min P0.01)。(3)IES组0min血糖下降13%(P0.02),OGTT血糖AUC减少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减轻体重:慢性IES在第8周减重10%(P0.05),但是对食欲没有明显影响(P0.05)。(4)HbA1c:IES明显降低HbA1c水平6%(P0.05),HbA1c的改变与体重减低无关(R~2=0.153,P0.05)。(5)血GLP-1和胰岛素水平:8周治疗末,IES组空腹和OGTT 30min,GLP-1水平明显高于Sham组。IES提高了30min血胰岛素水平(P0.05),但是没有改变胰岛素曲线下面积(P0.05)。(6)胰腺重量:Sham组体重标化的胰腺重量明显低于WKY组(P0.05)。而IES组胰腺重量与WKY组无差异。(7)胰岛的形态和功能:在一定范围内,慢性IES可提高胰岛β细胞数量,恢复胰岛的形态和结构,调节α和β细胞比例。四、结论1、自发性高血糖和胰高血糖素诱导的高血糖状态,均导致小肠肌电活动障碍。自主神经功能损害可能参与了高糖诱导的小肠电节律紊乱。2、急性IES:可降低2型糖尿病大鼠糖负荷后血糖。其降糖作用可能通过GLP-1介导。胃肠动力和自主神经调控均参与了IES的作用。3、慢性IES:可降低餐后及空腹血糖,其降糖作用可能通过调控GLP-1分泌、改善胰岛β细胞功能实现。
[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.
【学位授予单位】：南京医科大学
【学位级别】：博士
【学位授予年份】：2015
【分类号】：R587.1
本文编号：2169438
[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.
【学位授予单位】：南京医科大学
【学位级别】：博士
【学位授予年份】：2015
【分类号】：R587.1
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