The etiopathogenesis of the autoimmune disease type 1 diabetes (T1D) is still largely unknown, however, both genetic and environmental factors contribute to the development of the disease. A major contact surface for environmental factors is the gastrointestinal (GI) tract, where barrier defects in T1D likely cause diabetogenic antigens to enter the body tissues, contributing to beta-cell autoimmunity. Human and animal research imply that increased intestinal permeability is an important disease determinant, although the underlying methodologies, interpretations and conclusions are diverse. In this review, an updated comprehensive overview on intestinal permeability in patients with T1D and animal models of T1D is provided in the categories: in vivo permeability, ex vivo permeability, zonulin, molecular permeability and blood markers. Across categories, there is consistency pointing towards increased intestinal permeability in T1D. In animal models of T1D, the intestinal permeability varies with age and strains implying a need for careful selection of method and experimental setup. Furthermore, dietary interventions that affect diabetes incidence in animal models does also impact the intestinal permeability, suggesting an association between increased intestinal permeability and T1D development.

自身免疫性疾病 1 型糖尿病 (T1D) 的发病机制在很大程度上仍是未知的，然而，遗传和环境因素都有助于该疾病的发展。环境因素的主要接触表面是胃肠道，其中 T1D 中的屏障缺陷可能导致致糖尿病抗原进入身体组织，从而导致 β 细胞自身免疫。人类和动物研究表明，增加的肠道通透性是一个重要的疾病决定因素，尽管潜在的方法、解释和结论是多种多样的。在这篇综述中，在以下类别中提供了关于 T1D 患者肠道通透性和 T1D 动物模型的最新综合概述：体内通透性、离体通透性、连蛋白、分子通透性和血液标志物。在各个类别中，一致表明 T1D 肠道通透性增加。在 T1D 的动物模型中，肠道通透性随年龄和菌株而变化，这意味着需要仔细选择方法和实验设置。此外，在动物模型中影响糖尿病发病率的饮食干预措施也会影响肠道通透性，这表明肠道通透性增加与 T1D 发展之间存在关联。