期刊
DIABETES
卷 62, 期 5, 页码 1676-1680出版社
AMER DIABETES ASSOC
DOI: 10.2337/db12-1207
关键词
-
资金
- JDRF [2008-1012, 2007-502, 2007-1059, 2006-351]
- National Institutes of Health [R01 DK057846, P30 DK20495, UL1 RR024139, UL1 RR025780, UL1 RR024131, UL1 RR024134]
- Howalt family
- Tobacco Trust Fund
- Department of Public Health, State of Connecticut [2012-0222]
Type 1 diabetes (T1D) results from immune-mediated destruction of insulin-producing beta-cells. The killing of beta-cells is not currently measurable; beta-cell functional studies routinely used are affected by environmental factors such as glucose and cannot distinguish death from dysfunction. Moreover, it is not known whether immune therapies affect killing. We developed an assay to identify beta-cell death by measuring relative levels of unmethylated INS DNA in serum and used it to measure beta-cell death in a clinical trial of teplizumab. We studied 43 patients with recent-onset T1D, 13 nondiabetic subjects, and 37 patients with T1D treated with FcR nonbinding anti-CD3 monoclonal antibody (teplizumab) or placebo. Patients with recent-onset T1D had higher rates of beta-cell death versus nondiabetic control subjects, but patients with long-standing T1D had lower levels. When patients with recent-onset T1D were treated with teplizumab, beta-cell function was preserved (P < 0.05) and the rates of beta-cell were reduced significantly (P < 0.05). We conclude that there are higher rates of beta-cell death in patients with recent-onset T1D compared with nondiabetic subjects. Improvement in C-peptide responses with immune intervention is associated with decreased beta-cell death. Diabetes 62:1676-1680, 2013
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据