CENTER OF EXCELLENCE IN DIABETES AND OBESITY RESEARCH: PROJECT 1

该子项目是利用 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来源获得主要资金， 因此可以在其他CRISP条目中表示。列出的机构是 中心，不一定是研究者的机构。 糖尿病的并发症之一是在细胞中产生过量的活性氧（ROS）。 ROS是高活性的含氧分子，其可以破坏蛋白质或核酸，从而导致细胞死亡或功能异常。过量的ROS对心血管组织特别有害。ROS作为代谢葡萄糖的蛋白质的副产物产生，并且通常在具有正常血糖的个体中不是问题。然而，在糖尿病个体中，这些代谢酶被压倒，导致过量的ROS。细胞通常具有抵消过量ROS产生的机制，包括一氧化氮（NO），其水平与ROS成反比。然而，在糖尿病条件下，NO水平也降低，这增加了氧化损伤的可能性。因此，在本项目中，我们将利用糖尿病小鼠模型，探索抵消高ROS水平的机制。

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. One of the complications of diabetes is the production of excess reactive oxygen species (ROS) in cells. ROS are highly reactive oxygen-containing molecules that can damage proteins or nucleic acids thereby resulting in cell death or abnormal function. Excess ROS are particularly harmful for cardiovascular tissues. ROS are produced as by products of proteins which metabolize glucose and are generally not a problem in individuals with normal blood glucose. In diabetic individuals however, these metabolizing enzymes are overwhelmed and excess ROS results. A cell normally has mechanisms to counteract excess ROS production including nitric oxide (NO), whose levels are inversely proportional to ROS. In diabetic conditions however, NO levels are also decreased which enhances the possibility of oxidative damage. In this project therefore we will utilize mouse models of diabetes and explore mechanisms to counteract high ROS levels.