This subproject is one of many research subprojects utilizing theresources provided by a Center grant funded by NIH/NCRR. The subproject andinvestigator (PI) may have received primary funding from another NIH source,and thus could be represented in other CRISP entries. The institution listed isfor the Center, which is not necessarily the institution for the investigator.Type 1 diabetes mellitus is an immune-mediated disease in which insulin-producing beta cells are completely destroyed resulting in life-long dependence on exogenous insulin, which is increasing each year and is approaching an epidemic level in some countries that track this information. Beta cell destruction generally begins years before clinical onset as identified by the presence of circulating autoantibodies for disease relevant antigens. Though impairment in beta cell function is detected prior to clinical diagnosis, patients with Type 1 diabetes retain a significant amount of beta cell function as measured by C-peptide responses to a mixed meal tolerance test MMTT. Affected individuals often enter a honeymoon or remission phase where this insulin secretion is also seen. However, beta cell function deteriorates after diagnosis, eventually becoming undetectable and necessitating increasing reliance on exogenous insulin replacement. In the non-obese diabetic NOD mouse model of Type 1 Diabetes Mellitus T1DM, it has been demonstrated that the oral administration of islet autoantigens is effective in delaying the onset of T1DM. In the recently completed Type 1 Diabetes Prevention Trial DPT-1, oral insulin appeared to be effective in delaying the onset of T1DM in a subset of relatives at-risk for the disease. The primary objective of this study is to determine whether intervention with repeated oral administration of recombinant human insulin will prevent or delay development of clinical Type 1 Diabetes Mellitus in subjects at risk for T1DM.
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