Secondary Logo

Journal Logo

Institutional members access full text with Ovid®

The gut microbiota in type 1 diabetes

friend or foe?

Gavin, Patrick G.; Hamilton-Williams, Emma E.

Current Opinion in Endocrinology, Diabetes and Obesity: August 2019 - Volume 26 - Issue 4 - p 207–212
doi: 10.1097/MED.0000000000000483
DIABETES AND ENDOCHRINE PANCREAS II: Edited by Peter A. Gottlieb
Buy

Purpose of review 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.

Recent findings 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.

Summary 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.

The University of Queensland Diamantina Institute, The University of Queensland, Woolloongabba, Queensland, Australia

Correspondence to Emma E. Hamilton-Williams, The University of Queensland Diamantina Institute, The University of Queensland, 37 Kent St, Woolloongabba, Brisbane 4102, QLD, Australia. E-mail: e.hamiltonwilliams@uq.edu.au

Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.