NEUROPATHY ASSOCIATED WITH IMPAIRED GLUCOSE TOLERANCE

与葡萄糖耐量受损相关的神经病

• 批准号: 7718493
• 负责人: John Robinson Singleton
• 金额: $ 0.34万
• 依托单位: UNIVERSITY OF UTAH
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-03-01 至 2008-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7718493
• 关键词: Age; Clinical; Computer Retrieval of Information on Scientific Projects Database; Count; Defect; Developed Countries; Developing Countries; Diabetes Mellitus; End Point; Epidemiologic Studies; Fiber; Frequencies; Funding; General Population; Glucose; Grant; Histologic; Hyperglycemia; Institution; Insulin Resistance; Measures; Morbidity - disease rate; Natural History; Nerve Fibers; Neurologic; Neuropathy; Pain; Patients; Peripheral Nervous System Diseases; Phenotype; Pilot Projects; Reporting; Research; Research Personnel; Resources; Source; Syndrome; United States National Institutes of Health; cardiovascular risk factor; diet and exercise; double-blind placebo controlled trial; glucose metabolism; impaired glucose tolerance; prevent; prospective; sensory neuropathy

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Sensory neuropathy, often with pain, is a common neurologic problem. In developed countries, type II (insulin resistant) diabetes is the most frequently defined cause of sensory neuropathy. We have found that 35-50% of prospectively evaluated patients with otherwise idiopathic painful peripheral neuropathy have impaired glucose tolerance (IGT), an intermediate defect in glucose metabolism which correlates with insulin resistance syndrome, and has been shown to carry an independent risk for cardiovascular morbidity. This is a significantly greater frequency of IGT than reported in large epidemiologic studies of age matched general population (14%). We hypothesize that the postprandial hyperglycemia identified by IGT causes or contributes to a painful, small fiber neuropathy that is indistinguishable from that observed in early frank diabetes, and that early, aggressive treatment of IGT patients to normalize hyperglycemia will slow or prevent progression of neuropathy. This clinical pilot study will lay the groundwork for a later prospective double blind placebo controlled trial of patients with IGT and neuropathy to determine if treatment with intensive diet and exercise cousneling, or a glucose loweing agent can stabilize or reverse neuropathy. In this initial study we will: Characterize the clinical, electrodiagnostic, and histologic phenotype of neuropathy associated with IGT. Define the natural history of IGT associated neuropathy progression using validated endpoint measures, and Validate the use of intraepidermal nerve fiber counting (IENF) as a measure of small fiber loss.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 感觉神经病，通常伴有疼痛，是一种常见的神经系统问题。在发达国家，II 型（胰岛素抵抗）糖尿病是感觉神经病最常见的病因。我们发现，经过前瞻性评估的特发性疼痛性周围神经病患者中有 35-50% 患有糖耐量受损 (IGT)，这是一种与胰岛素抵抗综合征相关的葡萄糖代谢中间缺陷，并且已被证明具有心血管发病的独立风险。与年龄匹配的一般人群的大型流行病学研究中报告的 IGT 发生率相比 (14%) 显着更高。我们假设 IGT 识别的餐后高血糖会导致或促成疼痛性小纤维神经病，这种病与早期糖尿病中观察到的情况无法区分，并且对 IGT 患者进行早期积极治疗以使高血糖正常化将减缓或防止神经病的进展。这项临床试点研究将为以后对 IGT 和神经病变患者进行前瞻性双盲安慰剂对照试验奠定基础，以确定强化饮食和运动咨询或降血糖药物的治疗是否可以稳定或逆转神经病变。在这项初步研究中，我们将： 描述与 IGT 相关的神经病变的临床、电诊断和组织学表型特征。 使用经过验证的终点测量来定义 IGT 相关神经病进展的自然史，以及 验证使用表皮内神经纤维计数 (IENF) 作为小纤维损失的测量方法。