ESPE Abstracts

Introduction: Type 1 Diabetes (T1D) is an autoimmune disease where β-cells of the pancreatic islets are destroyed. The vast majority of T1D cases are not due to genetic predisposition, implying that the prevalence is associated with environmental, nongenetic factors. One such factor is the microbiome and its correlation with T1D has been investigated in a multitude of studies.

Aims: To investigate whether the current literature is providing evidence that there is a link between onset of T1D and the microbiome.

Methods and materials: Search for primary literature was done using PubMed Central.

Changes in the gut microbial communities Two of the main factors identified that have the capacity to change the microbial diversity are age and cessation of breastfeeding. Breastfeeding is selective for lactose degrading bacteria, while incorporation of fibre is aided by transketolase. Because of this, the fluctuations in the microbial communities during this transitional period is evident.

A positive correlation associated with predisposed T1D child was found between Blautia, Ruminococcus, Rikenellaceae and Streptococcus genera outgrowth even prior to disease onset. Some species within these genera are described as pathobionts, potentially causing inflammation. Significant correlation was found between increase of Bacteroides and anti-islet antibodies.

Gut integrity was also compromised in pre-T1D cases, as butyrate producing bacteria were low. Butyrate is especially important as it maintains the gut epithelial stability and ensures bacterial localisation. Additionally, there was an observation of increased production of triglycerides and branched-chain amino acids from Blautia and Ruminococcus.

Discussion: Cessation of breastfeeding and age are linked, as reduction in breastmilk and incorporation of solid foods on the basis on age of the child, which in turn induces the changes in the microbiome. The presence of Blautia, Ruminococcus, Rikenellaceae and Streptococcus in pre-T1D children cannot only cause gut inflammation but also induce permeability of the gut, which can be aided by the reduced number of butyrate, during which microorganisms can reside in the intraperitoneal space, causing increase in inflammation. Moreover, the increase of triglycerides pre- and post-T1D onset increases the unpredictability of hypoglycaemia. The positive correlation between Bacteroides and anti-islet antibodies advances the further destruction of β-cells and aiding disease onset.

Conclusion: It is evident that the gut microbiome has an effect on T1D onset and progression, with these findings highlight the importance of understanding the microbiome of T1D, which can potentially aid treatment, diagnosis and perhaps even prevention.