NEUROPATHY ASSOCIATED WITH IMPAIRED GLUCOSE TOLERANCE

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子项目和研究者（PI）可能从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。所列机构为中心，不一定是研究者所在机构。感觉神经病，通常伴有疼痛，是一种常见的神经系统疾病。在发达国家，2型糖尿病是感觉神经病变最常见的明确原因。 在大约40%的神经病变患者中，无法确定病因（？特发性神经病？）。我们和其他人已经表明，35-50%的特发性神经病患者有糖耐量受损（IGT），而年龄匹配的一般人群中只有14%。IGT定义为2小时口服葡萄糖耐量试验（OGTT）后葡萄糖水平在140和200 mg/dL之间，空腹血糖低于126 mg/dL。IGT患者几乎一致具有疼痛性感觉神经病变，将其与早期糖尿病神经病变的表型联系起来。 糖尿病控制和并发症试验（DCCT）清楚地表明，神经病变的发作和严重程度与I型糖尿病的血糖控制相关。在DCCT中，高血糖症的积极治疗预防或减缓了神经病变的进展，而糖尿病预防计划（DPP）表明，强化饮食和运动调整可以预防从IGT进展为糖尿病，并为IGT患者制定了护理标准。我们假设，发作性高血糖导致的神经病变在临床上与在坦率的糖尿病患者中观察到的神经病变难以区分，并且有必要进行积极的治疗以使血糖水平正常化，以减缓这些患者神经病变的进展。为了验证这一假设，我们提出了一项前瞻性对照试验，以确定强化饮食和运动咨询治疗是否可以稳定或逆转IGT患者的神经病变

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 2 diabetes is the most frequent defined cause of sensory neuropathy. In approximately 40% of patients with neuropathy, no cause can be defined (?idiopathic neuropathy?). We and others have shown that 35-50% of patients with otherwise idiopathic neuropathy have impaired glucose tolerance (IGT), compared to 14% of the age matched general population. IGT is defined as a glucose level after a 2 hour oral glucose tolerance test (OGTT) between 140 and 200 mg/dL and a fasting plasma glucose less than 126 mg/dL. Patients with IGT almost uniformly have a painful sensory neuropathy, linking them to the phenotype of early diabetic neuropathy. The Diabetes Control and Complications Trial (DCCT) clearly showed that neuropathy onset and severity correlates with glycemic control in type I diabetes. In the DCCT, aggressive treatment of hyperglycemia prevented or slowed the progression of neuropathy, while the Diabetes Prevention Program (DPP) shows that intensive diet and exercise modification can prevent progression from IGT to diabetes and sets a standard of care for IGT patients. We hypothesize that episodic hyperglycemia contributes to a neuropathy that is clinically indistinguishable from that observed in patients with frank diabetes, and that aggressive treatment to normalize blood glucose levels will be necessary to slow progression of neuropathy in these patients. To test this hypothesis, we propose a prospective controlled trial to determine if treatment with intensive diet and exercise counseling can stabilize or reverse neuropathy in IGT patients