MECHANISM OF DIABETIC CARDIOMYOPATHY

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。 在美国，随着患者数量的稳步增加，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. 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. Cardiomyopathy and heart failure secondary to type 2 diabetic mellitus (DM) is becoming an enormous hearth 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.