ESPE Abstracts

The conspicuous increase in the incidence of type 1 diabetes (T1D) in the Western world after World War II cannot be explained solely by genetic factors but suggests that this rise must be due to crucial interactions between predisposing genes and environmental changes. Three parallel phenomena in early childhood – the dynamic development of the immune system, the maturation of the gut microbiome and the appearance of the first T1D-associated autoantibodies – imply that these phenomena might reflect causative relationships. A lot of novel data on the role of the microbiome in the development of T1D has accumulated recently but proving causality has remained challenging. The gut microbiota plays definitely an important role in the training and maturation of the immune system. A dysbiotic intestinal microbiota including decreased microbial diversity, increased abundance of potentially pathogenic bacteria and a reduced number of functional genes have been reported to be characteristic features of children, who progress to clinical T1D. In the INNODIA study the gut microbiome of 98 individuals affected by TID were analysed at the time of diagnosis and 3, 6, 12 and 24 months later. The gut microbiome composition – both individual taxa and functional modules – varied between the participating 12 clinical sites. Relative abundances of several bacterial species, increased after the diagnosis of T1D. Several statistically significant associations were seen between the microbiome and clinical parameters, including insulin dose, fasting C-peptide and HbA1c. Increasing insights into the role of the gut microbiota in T1D will improve the possibilities to manipulate the microbiota to reduce the risk of T1D in risk individuals and to improve the metabolic control in patients with established disease. Microbial metabolites may be stronger tools for the manipulation of the intestinal microbiota than specific microbes.