The University of Queensland Diamantina Institute, The University of Queensland, Woolloongabba, Queensland, Australia.
Curr Opin Endocrinol Diabetes Obes. 2019 Aug;26(4):207-212. doi: 10.1097/MED.0000000000000483.
Evidence is mounting that disturbances in the gut microbiota play a role in the rising incidence of type 1 diabetes (T1D) and new technologies are expanding our ability to understand microbial function and host interactions. Longitudinal data from large cohorts of children at risk of T1D are nor solidifying our understanding of the function of the microbiota in this disease.
Although taxonomic changes in the gut microbiota associated with T1D are relatively modest, a functional defect in production of short-chain fatty acids (SCFAs) remains as a unifying feature across multiple studies and populations. Dysbiosis of the microbiota in T1D has been linked to decreased gut barrier and exocrine pancreas function. We explore factors contributing to the disturbed microbiota in T1D such as infant diet, probiotic use and genetic risk linked to defective immune regulation. We also discuss the interplay between immunotherapy, the gut immune response and the microbiota.
Functional alterations in the microbiota are linked to pathogenesis of T1D and these findings provide a rationale for future investigations aimed at establishing a healthy microbiota and promoting SCFA production and prevention of T1D.
越来越多的证据表明,肠道微生物群的紊乱在不断上升的 1 型糖尿病(T1D)发病机制中起着作用,新技术正在扩大我们理解微生物功能和宿主相互作用的能力。来自 T1D 高危儿童的大型队列的纵向数据正在巩固我们对微生物群在该疾病中的功能的理解。
尽管与 T1D 相关的肠道微生物群的分类变化相对较小,但在多个研究和人群中,短链脂肪酸(SCFAs)产生的功能缺陷仍然是一个统一的特征。T1D 中微生物群的失调与肠道屏障和外分泌胰腺功能下降有关。我们探讨了导致 T1D 中微生物群紊乱的因素,如婴儿饮食、益生菌使用以及与免疫调节缺陷相关的遗传风险。我们还讨论了免疫疗法、肠道免疫反应和微生物群之间的相互作用。
微生物群的功能改变与 T1D 的发病机制有关,这些发现为未来旨在建立健康的微生物群、促进 SCFA 产生和预防 T1D 的研究提供了依据。