Barbara Davis Center for Childhood Diabetes, University of Colorado Denver, 1775 Aurora Ct, Aurora, CO, 80045, USA.
Faculty of Medicine and Life Sciences, University of Tampere, Tampere, Finland.
Curr Diab Rep. 2018 Oct 23;18(12):136. doi: 10.1007/s11892-018-1113-2.
The environmental triggers of islet autoimmunity leading to type 1 diabetes (T1D) need to be elucidated to inform primary prevention. The Environmental Determinants of Diabetes in the Young (TEDDY) Study follows from birth 8676 children with T1D risk HLA-DR-DQ genotypes in the USA, Finland, Germany, and Sweden. Most study participants (89%) have no first-degree relative with T1D. The primary outcomes include the appearance of one or more persistent islet autoantibodies (islet autoimmunity, IA) and clinical T1D.
As of February 28, 2018, 769 children had developed IA and 310 have progressed to T1D. Secondary outcomes include celiac disease and autoimmune thyroid disease. While the follow-up continues, TEDDY has already evaluated a number of candidate environmental triggers, including infections, probiotics, micronutrient, and microbiome. TEDDY results suggest that there are multiple pathways leading to the destruction of pancreatic beta-cells. Ongoing measurements of further specific exposures, gene variants, and gene-environment interactions and detailed "omics" studies will provide novel information on the pathogenesis of T1D.
为了进行一级预防，需要阐明导致 1 型糖尿病（T1D）的胰岛自身免疫的环境触发因素。儿童糖尿病环境研究（TEDDY）是在美国、芬兰、德国和瑞典对出生时具有 T1D 风险 HLA-DR-DQ 基因型的 8676 名儿童进行的一项研究。大多数研究参与者（89%）没有一级亲属患有 T1D。主要结局包括出现一种或多种持续的胰岛自身抗体（胰岛自身免疫，IA）和临床 T1D。
截至 2018 年 2 月 28 日，769 名儿童出现了 IA，310 名儿童发展为 T1D。次要结局包括乳糜泻和自身免疫性甲状腺疾病。虽然随访仍在继续，但 TEDDY 已经评估了许多候选环境触发因素，包括感染、益生菌、微量营养素和微生物组。TEDDY 的结果表明，存在多种导致胰腺β细胞破坏的途径。正在对进一步的特定暴露、基因变异以及基因-环境相互作用进行测量，并进行详细的“组学”研究，这将为 T1D 的发病机制提供新的信息。
