Evaluating the Causal Role of Gut Microbiota in Type 1 Diabetes and Its Possible Pathogenic Mechanisms
Type 1 diabetes (T1D) is a multifactorial autoimmune disease mediated by genetic, epigenetic, and environmental factors. In recent years, the emergence of high-throughput sequencing has allowed us to investigate the role of gut microbiota in the development of T1D. Significant changes in the composi...
Saved in:
Published in | Frontiers in endocrinology (Lausanne) Vol. 11; p. 125 |
---|---|
Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Switzerland
Frontiers Media S.A
24.03.2020
|
Subjects | |
Online Access | Get full text |
ISSN | 1664-2392 1664-2392 |
DOI | 10.3389/fendo.2020.00125 |
Cover
Loading…
Summary: | Type 1 diabetes (T1D) is a multifactorial autoimmune disease mediated by genetic, epigenetic, and environmental factors. In recent years, the emergence of high-throughput sequencing has allowed us to investigate the role of gut microbiota in the development of T1D. Significant changes in the composition of gut microbiome, also termed dysbiosis, have been found in subjects with clinical or preclinical T1D. However, whether the dysbiosis is a cause or an effect of the disease remains unclear. Currently, increasing evidence has supported a causal link between intestine microflora and T1D development. The current review will focus on recent research regarding the associations between intestine microbiome and T1D progression with an intention to evaluate the causality. We will also discuss the possible mechanisms by which imbalanced gut microbiota leads to the development of T1D. |
---|---|
Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 ObjectType-Review-3 content type line 23 This article was submitted to Clinical Diabetes, a section of the journal Frontiers in Endocrinology Reviewed by: Carol Huang, University of Calgary, Canada; Hidetaka Hamasaki, Hamasaki Clinic, Japan Edited by: Jan Polák, Charles University, Czechia |
ISSN: | 1664-2392 1664-2392 |
DOI: | 10.3389/fendo.2020.00125 |