MECHANISM OF DIABETIC CARDIOMYOPATHY

这个子项目是利用资源的许多研究子项目之一。 由NIH/NCRR资助的中心拨款提供。对子项目的主要支持 子项目的首席调查员可能是由其他来源提供的， 包括美国国立卫生研究院的其他来源。为子项目列出的总成本可能 表示该子项目使用的中心基础设施的估计数量， 不是由NCRR赠款提供给次级项目或次级项目工作人员的直接资金。 在美国，随着患者人数的稳步增加，继发于2型糖尿病(DM)的心肌病和心力衰竭正成为一个巨大的健康问题。我们等人收集的证据表明，高血糖及其相关的代谢异常直接影响心肌细胞的收缩能力和能量利用，我们推测过度蛋白质糖基化导致的线粒体形态和生化缺陷是主要原因。该项目旨在利用糖尿病啮齿动物模型和先进的显微技术来确定长期高血糖引起的线粒体的解剖和功能变化。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. Cardiomyopathy and heart failure secondary to type 2 diabetic mellitus (DM) is becoming an enormous health issue in the US with a steady increase in patient population. Evidence collected by our groups and others now indicates that hyperglycemia and associated metabolic abnormalities directly affect the contractility and the energy usage of cardiomyocytes and we hypothesize morphological and biochemical defects of mitochondria induced by excessive protein glycosylation plays a major role. This project aims to determine anatomical and functional changes in mitochondria caused by prolonged hyperglycemia using rodent models of DM and advanced microscopic technologies.