MOLECULAR MECHANISMS OF HYPERGLYCEMIA AND DIABETES-INDUCED MONOCYTE ACT

本子项目是利用由NIH/NCRR资助的中心赠款提供的资源的众多研究子项目之一。子项目和研究者（PI）可能已经从另一个NIH来源获得了主要资金，因此可以在其他CRISP条目中表示。列出的机构是中心的，不一定是研究者的机构。本研究旨在确定导致I型和II型糖尿病人群心血管（心脏和血管）并发症发生率高（3-4倍）的机制。血液单核细胞粘附到血管壁上，迁移到血管中，并吸收脂肪颗粒，如胆固醇的坏部分，被称为低密度脂蛋白胆固醇，是血管堵塞的一些最早的事件，可能导致心脏病发作。本研究旨在确定高血糖水平（高血糖症）和高脂肪水平（高脂血症）如何使这些过程恶化。我们早期的研究表明，在高血糖条件下培养正常单核细胞可以改变基因，使它们表现异常。比较健康志愿者与I型和II型糖尿病患者分离的单核细胞可能有助于提高我们对疾病过程的理解。

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. This study is designed to determine the mechanisms responsible for the high rates (3-4 fold) of cardiovascular (heart and blood vessels) complications in the Type I and Type II diabetic population. The adhesion of blood monocytes to the vessel wall, migration into the blood vessel and uptake of fat particles, such as the bad fraction of cholesterol, known as LDL cholesterol, are some of the earliest events in the clogging of blood vessels which can lead to heart attacks. This study is designed to determine how elevated blood glucose levels (hyperglycemia) and high fat levels (hyperlipidemia) can worsen these processes. Our earlier studies have shown that culture of normal monocytes under hyperglycemia conditions can alter genes and make them behave abnormally. The comparison of isolated monocytes from healthy volunteers versus patients with Type I and Type II diabetes may help to improve our understanding of the disease process.