The role for gut permeability in the pathogenesis of type 1 diabetes--a solid or leaky concept?
The role for gut permeability in the pathogenesis of type 1 diabetes--a solid or leaky concept?
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DOI：
10.1111/pedi.12305
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发表时间：
2015-11
影响因子：
3.4
通讯作者：
Atkinson MA
中科院分区：
文献类型：
--
作者：
Li X;Atkinson MA
越来越多的证据，功能和形态学，支持增加肠道通透性的概念作为1型糖尿病（T1 D）在人类和动物模型的疾病的内在特征。通常被称为“漏肠”，其对T1 D发病机制的影响仍不清楚。假设这种缺陷影响对抗原（自身和非自身）的免疫反应占主导地位，但其他人认为高血糖症和胰岛炎可能导致T1 D肠道通透性增加。为了解决这些复杂的问题，我们在此回顾了漏肠在T1 D发病机制中的许多概念性作用，并提出了一些方法，如果是真的，针对肠-胰腺轴的治疗干预可能被证明是有前途的未来治疗干预。
Increasing evidence, both functional and morphological, supports the concept of increased intestinal permeability as an intrinsic characteristic of type 1 diabetes (T1D) in both humans and animal models of the disease. Often referred to as a “leaky gut”, its mechanistic impact on the pathogenesis of T1D remains unclear. Hypotheses that this defect influences immune responses against antigens (both self and non-self) predominate, yet others argue hyperglycemia and insulitis may contribute to increased gut permeability in T1D. To address these complicated issues, we herein review the many conceptual role(s) for a leaky gut in the pathogenesis of T1D and suggest ways that if true, therapeutic interventions aimed at the gut-pancreas axis may prove promising for future therapeutic interventions.