PATHOGENESIS OF HUMAN INSULIN DEPENDENT DIABETES

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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.