PATHOGENESIS OF HUMAN INSULIN DEPENDENT DIABETES

人类胰岛素依赖性糖尿病的发病机制

• 批准号: 7379301
• 负责人: JERRY P PALMER
• 金额: $ 0.5万
• 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/7379301
• 关键词: PATHOGENESIS; HUMAN; INSULIN; DEPENDENT; 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. This intervention study is testing whether one treatment is superior over another in the management of type 1.5 diabetes. Type 1 and Type 2 diabetes have different underlying causes. Type 1 is autoimmune in nature causing the destruction of pancreatic beta cells. Type 2 diabetes is not autoimmune. A third group which looks like type 2 but has the autoantibodies commonly seen in type 1 is called type 1.5. 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. This intervention study is comparing 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。这项干预研究正在测试一种治疗方法在1.5型糖尿病的管理中是否上级另一种治疗方法。1型糖尿病和2型糖尿病有不同的潜在原因。1型是自身免疫性的，导致胰腺β细胞的破坏。2型糖尿病不是自身免疫性的。第三组看起来像2型，但具有1型中常见的自身抗体，称为1.5型。与经典的2型糖尿病患者相比，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。这项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。