Gastroparesis Gastric Dysrhythmias and Dyspepsia Symp*

2型糖尿病（T2 DM）困扰着1400万患者;许多患者患有未确诊的胃轻瘫 (GP)并且遭受恶心、腹胀和腹部不适。本研究的主要目的是：1） 确定胃动力异常的患病率和遗传成分（例如GP，胃动力异常）， 2）研究T2 DM同胞对中的心律失常）和消化不良样症状; 2）研究 急性激发试验餐期间的消化不良症状和胃动力障碍;以及3）确定 治疗高血糖对消化不良症状和胃动力障碍的影响。具体目标 是：1）确定消化不良症状，GP和胃节律紊乱的患病率，在一个大的，良好的- 目前入组NIH的T2 DM同胞对的特征性社区人群 申办的研究; 2）将人口统计学、症状、实验室检查结果、胃动力试验数据相关联，以及 2型糖尿病伴和不伴糖蛋白同胞对的遗传成分; 3）探讨糖蛋白的发病机制 和消化不良症状通过测量胃肌电活动和选择的激素（例如，胃饥饿素， 胆囊收缩素和加压素）对刺激性试验餐的反应;以及4）确定 积极的血糖控制对消化不良症状和胃动力功能的影响。研究设计 纳入了从1200例充分表征的T2 DM患者的数据库中招募的200对同胞对。 症状问卷、固相胃排空研究和胃电图记录， 激发性试验餐将在5年内完成（长期研究）。从这些 研究将确定胃病和消化不良症状的患病率， 大量T2 DM患者。一个有和没有GP的T2 DM患者亚组将接受非侵入性 在刺激性水负荷试验和热量餐试验期间进行生理测试和激素测定。结果 这些研究将为T2 DM患者的餐后症状提供新的见解， GP.在短期研究中，GP和HbA 1c>8的患者将接受积极治疗，以获得正常 6个月期间的血糖水平和HbA 1c水平，并与 胃排空正常，HbA 1C <8。无热量和热量餐试验的胃电图试验 在治疗3个月和6个月后重复进行胃排空试验，并在治疗6个月后进行固相胃排空试验。 短期研究的结果将表明高血糖症与症状、胃肠道功能和糖尿病的相关性。 T2 DM患者中的心律失常和GP。在美国有T2 DM的流行， 患者具有未被识别的胃动力障碍。拟议的研究将确定 2型糖尿病患者的“糖尿病胃”，探讨消化不良症状和胃 神经肌肉功能障碍，并评估高血糖在胃运动功能障碍中的作用。

Type 2 diabetes mellitus (T2DM) afflicts 14 million patients; many patients have undiagnosed gastroparesis (GP) and suffer from nausea, bloating, and abdominal discomfort. Broad objectives of this study are to: 1) determine the prevalence and heritable components of gastric motility abnormalities (e.g. GP, gastric dysrhythmias) and dyspepsia-like symptoms in sibling pairs with T2DM; 2) investigate mechanisms of dyspepsia symptoms and gastric motility dysfunction during acute provocative test meals; and 3) determine the effect of treatment of hyperglycemia on dyspepsia symptoms and gastric motility disorders. Specific aims are: 1) to determine the prevalence of dyspepsia symptoms, GP, and gastric dysrhythmias in a large, well- characterized, community-based population of sibling pairs with T2DM currently enrolled in an NIH sponsored study; 2) to correlate demographics, symptoms, laboratory results, gastric motility test data, and hereditable components in sibling pairs with T2DM with and without GP; 3) to investigate mechanisms of GP and dyspepsia symptoms by measuring gastric myoelectrical activity and selected hormones (e.g., ghrelin, cholecystokinin, and vasopressin) in response to provocative test meals; and 4) to determine the effect of aggressive glucose control on dyspepsia symptoms and gastric motility function. Research design incorporates the recruitment of 200 sibling pairs from a data base of 1200 well-characterized T2DM patients. Symptom questionnaires, solid-phase gastric emptying studies and electrogastrogram recordings with provocative test meal will be completed over the 5 year period (Long-Term Study). Results from these studies will determine the prevalence of gastropathies and dyspepsia symptoms in a comprehensive study of a large population with T2DM. A subset of T2DM patients with and without GP will undergo non-invasive physiologic testing and hormone assays during a provocative water load test and a caloric meal test. Results of these studies will provide new insights into postprandial symptoms in patients with T2DM with and without GP. In the Short-Term Study, patients with GP and HbA1c >8 will be treated aggressively to obtain normal glucose levels and HbA1c levels during a 6 month time period and compared with T2DM patients with normal gastric emptying and HbA1C <8. Electrogastrogram testing with non-caloric and caloric meal tests will be repeated after 3 and 6 months and solid-phase gastric emptying tests after 6 months of therapy. Results from the Short-Term Study will indicate the relevance of hyperglycemia on symptoms, gastric dysrhythmias, and GP in patients with T2DM. There is an epidemic of T2DM in the United States and many patients have unrecognized stomach motility disorders. The proposed research will determine prevalence of the "diabetic stomach" in patients with T2DM, investigate mechanisms of dyspepsia symptoms and stomach neuromuscular dysfunction, and evaluate the role of hyperglycemia in stomach motility dysfunction.