Bacterial Interactions in the Gut May Influence Type 1 Diabetes
GAINESVILLE, FL – Our microbes outnumber our cells by 10 to 1. Especially in the lining of our gut, those microbes can be friends that help deliver nutrients or foes that cause pain and disease. A new study co-authored by University of Florida diabetes researchers underscores the role of these microbes, the so-called microbiome, in the pathogenesis of metabolic diseases such as diabetes.
Researchers from the University of Florida, along with the Institute of Diabetes Research, Helmholtz Zentrum Munchen, Germany, studied the gut bacteria of 44 children from infancy to age three (from the JDRF-funded BABYDIET study). During the course of the study, scientists compared the composition and interaction of the gut microbiota in children who went on to develop type 1 diabetes (T1D)-specific autoantibodies in their blood with data from children who were autoantibody negative.
They found that certain colonies of gut bacteria were for some reason uncommunicative and more physically isolated from other bacterial species in the group of children with T1D autoantibodies. These bacteria did not display the mutual interactions that appear to occur in those without anti-islet autoantibodies, regardless of bacterial abundance or diversity. The findings revealed that not only the microbial composition but also the way in which bacteria interacts in functional communities in the gut could affect the body’s immune system and may combine with certain environmental triggers to contribute to the pathogenesis of T1D.
Future research is now needed to include study participants without a familial predisposition to T1D, to clarify the possible causes of this phenomenon, and discover how these findings are related to the immune system defects and autoimmunity associated with T1D. These next steps could lead to novel prevention therapies for people at risk of developing the disease.
Endesfelder, D. et al. (2014): Compromised gut microbiota networks in children with anti-islet cell autoimmunity, Diabetes, published ahead of print March 7, 2014, doi:10.2337/db13-1676 1939-327X