PATHOGENESIS OF HUMAN TYPE 1 DIABETES

人类 1 型糖尿病的发病机制

• 批准号: 7379373
• 负责人: JERRY P PALMER
• 金额: $ 0.08万
• 依托单位: UNIVERSITY OF WASHINGTON
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-04-01 至 2007-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7379373
• 关键词: PATHOGENESIS; HUMAN; TYPE; DIABETES

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 purpose of this project is to determine: 1) The predictive value of islet cell antibodies and insulin autoantibodies in identifying individuals with beta cell dysfunction among non-diabetics. 2) The pattern of change in beta cell function over time in individuals positive for one or more of the above immunologic markers. 3) Whether one treatment is superior over another in the management of type 1.5 diabetes. Type 1.5 diabetes looks like type 2 but has the autoantibodies commonly seen in type 1. Compared to classic type 2 patients, type 1.5 diabetes has a more rapid decline in beta cell function, fails sulfonylurea therapy and requires insulin therapy earlier. The intervention study under purpose #3 compares rosiglitazone to glyburide to determine which study drug results in better preservation of beta cell function in patients with type 1.5 diabetes.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。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。所列机构为中心，不一定是研究者所在机构。本研究的目的是确定：1）胰岛细胞抗体和胰岛素自身抗体在非糖尿病患者中识别β细胞功能障碍个体的预测价值。2)在一种或多种上述免疫标志物阳性的个体中，β细胞功能随时间变化的模式。3)在1.5型糖尿病的管理中，一种治疗方法是否上级另一种。1.5型糖尿病看起来像2型糖尿病，但具有1型糖尿病常见的自身抗体。与经典的2型患者相比，1.5型糖尿病的β细胞功能下降更快，磺脲类药物治疗失败，需要更早的胰岛素治疗。目的#3下的干预研究比较了罗格列酮和格列本脲，以确定哪种研究药物能更好地保护1.5型糖尿病患者的β细胞功能。