IMPAIRED GLUCOSE TOLERANCE CAUSES NEUROPATHY
葡萄糖耐量受损导致神经病
基本信息
- 批准号:7603724
- 负责人:
- 金额:$ 0.34万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2007
- 资助国家:美国
- 起止时间:2007-03-01 至 2007-09-16
- 项目状态:已结题
- 来源:
- 关键词:AgeClinicalComputer Retrieval of Information on Scientific Projects DatabaseCounselingDefectDeveloped CountriesDeveloping CountriesDiabetes MellitusEpidemiologic StudiesFiberFrequenciesFundingGeneral PopulationGlucoseGrantHyperglycemiaInstitutionInsulin ResistanceMorbidity - disease rateNeurologicNeuropathyPainPatientsPeripheral Nervous System DiseasesPilot ProjectsReportingResearchResearch PersonnelResourcesSourceSyndromeUnited States National Institutes of Healthcardiovascular risk factordiet and exercisedouble-blind placebo controlled trialglucose metabolismimpaired glucose tolerancepreventprospectivesensory neuropathy
项目摘要
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.'
这个子项目是许多研究子项目中利用
资源由NIH/NCRR资助的中心拨款提供。子项目和
调查员(PI)可能从NIH的另一个来源获得了主要资金,
并因此可以在其他清晰的条目中表示。列出的机构是
该中心不一定是调查人员的机构。
感觉神经病,通常伴有疼痛,是一种常见的神经学问题。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明确原因。我们发现,在前瞻性评估的特发性痛性周围神经病患者中,有35-50%患有糖耐量减低(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,已被证明是心血管疾病的独立风险因素。这比在年龄匹配的普通人群的大型流行病学研究中报告的IGT的频率(14%)要高得多。我们假设,IGT发现的餐后高血糖会导致或导致疼痛的细小纤维神经病,这与早期弗兰克糖尿病时观察到的没有区别,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。这项临床先导性研究将为后来对IGT和神经病变患者进行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剂是否可以稳定或逆转神经病变。
项目成果
期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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JAMES W RUSSELL其他文献
JAMES W RUSSELL的其他文献
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{{ truncateString('JAMES W RUSSELL', 18)}}的其他基金
ShEEP Request for Autonomic Nervous System Integrated Evaluation Laboratory
ShEEP 请求建立自主神经系统综合评价实验室
- 批准号:
9361301 - 财政年份:2017
- 资助金额:
$ 0.34万 - 项目类别:
NAD+ and SIRT1 Regulate Mitochondrial Function in Diabetic Neuropathy
NAD 和 SIRT1 调节糖尿病神经病变中的线粒体功能
- 批准号:
9174947 - 财政年份:2016
- 资助金额:
$ 0.34万 - 项目类别:
NAD+ and SIRT1 Regulate Mitochondrial Function in Diabetic Neuropathy
NAD 和 SIRT1 调节糖尿病神经病变中的线粒体功能
- 批准号:
10406480 - 财政年份:2016
- 资助金额:
$ 0.34万 - 项目类别:
Improving Autonomic Function and Balance in Diabetic Neuropathy
改善糖尿病神经病变的自主功能和平衡
- 批准号:
8990869 - 财政年份:2013
- 资助金额:
$ 0.34万 - 项目类别:
Improving Autonomic Function and Balance in Diabetic Neuropathy
改善糖尿病神经病变的自主功能和平衡
- 批准号:
9108883 - 财政年份:2013
- 资助金额:
$ 0.34万 - 项目类别:
SIRT1 Overexpression in Cellular Mitochondrial Metabolism and Function
SIRT1 在细胞线粒体代谢和功能中的过表达
- 批准号:
7449824 - 财政年份:2008
- 资助金额:
$ 0.34万 - 项目类别:
Oxidative Stress Induces Apoptosis in Diabetic Neurons
氧化应激诱导糖尿病神经元凋亡
- 批准号:
6365183 - 财政年份:2002
- 资助金额:
$ 0.34万 - 项目类别:
Oxidative Stress Induces Apoptosis in Diabetic Neurons
氧化应激诱导糖尿病神经元凋亡
- 批准号:
6821356 - 财政年份:2002
- 资助金额:
$ 0.34万 - 项目类别:
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