IMPAIRED GLUCOSE TOLERANCE CAUSES NEUROPATHY

葡萄糖耐量受损导致神经病

• 批准号: 7376534
• 负责人: JAMES W RUSSELL
• 金额: $ 4.55万
• 依托单位: UNIVERSITY OF MICHIGAN AT ANN ARBOR
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-04-05 至 2007-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7376534
• 关键词: aging; counseling; diet; exercise; glucose; glucose metabolism; glucose tolerance; hyperglycemia; insulin; insulin sensitivity /resistance; pain; placebos; sensory neuropathy; syndrome

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 frequent 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 the 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 counseling, or a glucose lowering agent can stabilize or reverse neuropathy.

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。感觉神经病变是一种常见的神经系统疾病，常伴有疼痛。在发达国家，II型（胰岛素抵抗）糖尿病是感觉神经病变最常见的病因。我们发现，35-50%的前瞻性评估的特发性疼痛周围神经病变患者有糖耐量（IGT）受损，这是一种与胰岛素抵抗综合征相关的糖代谢的中间缺陷，并且已被证明具有心血管疾病的独立风险。这明显高于年龄匹配普通人群的大型流行病学研究报告（14%）。我们假设，由IGT识别的餐后高血糖导致或促成了与早期糖尿病患者观察到的疼痛的小纤维神经病变，并且早期积极治疗IGT患者以使高血糖正常化将减缓或防止神经病变的进展。这项临床先导研究将为随后的IGT和神经病变患者的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糖药物治疗是否可以稳定或逆转神经病变。