POSTPRANDIAL HYPERGLYCEMIA

餐后高血糖

• 批准号: 7716618
• 负责人: David S Schade
• 金额: $ 0.48万
• 依托单位: UNIVERSITY OF NEW MEXICO
• 依托单位国家: 美国
• 财政年份: 2008
• 资助国家: 美国
• 起止时间: 2008-05-01 至 2008-11-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7716618
• 关键词: Cardiovascular Diseases; Computer Retrieval of Information on Scientific Projects Database; Development; Diabetes Mellitus; Dinoprost; Electron Transport; Epidemiologic Studies; F2-Isoprostanes; Funding; Glucose; Grant; Hyperglycemia; Incidence; Individual; Institution; Link; Mitochondria; Oral; Oxidative Stress; Production; Research; Research Personnel; Resources; Role; Source; Superoxides; United States National Institutes of Health; cardiovascular risk factor; diabetic; glycemic control; interest

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. The incidence of long term complications in diabetes has been strongly linked to glycemic control 1,2,3. Recently there has been significant interest in the role of postprandial hyperglycemia in the development of cardiovascular disease in diabetes 4,5,6. Epidemiological studies show a relationship between the 2hr glucose concentration after an oral load, and cardiovascular risk 7. In addition interventional studies aimed at reducing postprandial glucose concentrations, seem to support the importance of postprandial hyperglycemia as a target for diabetic therapy 8,9. Hyperglycemia has been shown to induce superoxide production by mitochondrial electron transport chain.This has been proposed as the underlying mechanism by which hyperglycemia leads to increased cardiovascular disease 10 F2 isoprostane 8-iso prostaglandin F2alpha, has been shown to be a reliable marker of oxidative stress 11,12. While there is a growing body of evidence in support of the importance of postprandial hyperglycemia as a target for diabetic treatment, many questions remained unanswered. In particular, it is not known whether it is the degree of hyperglycemia, or the duration for which an individual remains hyperglycemic, which results in the oxidative stress seen after a meal.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。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 研究中心，而研究中心不一定是研究者所在的机构。 糖尿病长期并发症的发生率与 血糖控制123最近，人们对 餐后高血糖在糖尿病心血管疾病发展中的作用4，5，6.流行病学研究表明， 口服负荷后2小时葡萄糖浓度和心血管风险7. 此外，旨在降低餐后血糖浓度的干预性研究似乎支持餐后高血糖作为糖尿病治疗目标的重要性8，9。高血压已被证明会诱导 线粒体电子传递链产生超氧化物。 被认为是高血糖导致增加的 心血管疾病10 F2异前列腺素8-异前列腺素F2 α， 已被证明是氧化应激的可靠标志物11，12。 虽然有越来越多的证据表明， 餐后高血糖作为糖尿病治疗的目标， 仍然没有答案。特别是，尚不清楚是高血糖的程度，还是个体保持高血糖的持续时间，导致餐后观察到的氧化应激。