Gut Microbes Differ in Young Children With Type 1 Diabetes

Lara C. Pullen, PhD

June 13, 2014

A new, albeit small, study from Europe indicates that very young children with type 1 diabetes appear to lack the bacterial species that are responsible for producing a beneficial metabolite from food, called butyrate, which in turn protects the gut from inflammation.

It is thought that this inflammation could trigger an immune response, say Marcus C. de Goffau, PhD, from the department of medical microbiology, University of Groningen, the Netherlands, and colleagues in their paper published online June 12 in Diabetologia.

"It appears as if diabetic children are one 'step' behind in their gut microbial development and that this development goes in an aberrant direction," he and his colleagues say.

They found that healthy children had a higher abundance of the butyrate-producing species of Clostridium clusters IV and XIVa, compared with the children who developed type 1 diabetes. The latter were more likely to have streptococci and Bacteroidetes in their stool samples.

"In microbiota, a very important word here is balance," Dr. de Goffau explained to Medscape Medical News. He stressed, however, that the study was designed to address correlation and doesn't prove causation.

Little Known About Gut Microbiota in Very Young Children

Dr. de Goffau and colleagues explain that the first years of life are the time when the intestinal microbiota develops most rapidly. While recent studies indicate that an aberrant gut microbiota is associated with the development of type 1 diabetes, little is known about the gut bacterial environment in children who have diabetes at an early age.

The aim of this study was to compare the gut microbiota of 1- to 5-year-old diabetic children with that of age-matched nondiabetic control children using the Human Intestinal Tract Chip (HITChip), a phylogenetic microarray that provides a deep global compositional analysis of the human intestinal microbiota.

They used fecal samples from 28 children newly diagnosed with type 1 diabetes and 27 controls, collected by parents at home and shipped at ambient temperature to the laboratory, where they were subsequently stored at -75°C.

The investigators compared 26 pairs of children (case and control, age-matched).

"Contrary to expectations, bifidobacteria were not found to be correlated with diabetes in this study of new-onset diabetes, even though they have previously been found to be negatively associated with beta-cell autoimmunity" in previous studies in older children (4 years and older), the researchers note.

But retaining a moderate bifidobacterial abundance as children grow older "might be more important in relation to type 1 diabetes" than the abundance of this species in young children, whose bifidobacterial levels are likely to be still high enough overall, they point out.

Instead, within the paired children younger than 2.9 years, children with diabetes had more streptococci and Bacteroidetes. In contrast, the combined abundance of Clostridium clusters IV and XIVa was higher in the healthy controls at this age.

Analysis of the children older than 2.9 years revealed that controls had a higher fraction of butyrate-producing species within Clostridium clusters IV and XIVa than did children with diabetes.

The study builds on previous research that found that Clostridium clusters IV and XIVa were important predictors in Finnish children for development of 2 or more diabetes-related autoantibodies, the authors explain.

In addition, multiple studies in humans and animal models have described an association between Bacteroidetes and diabetes, say Dr. de Goffau and colleagues.

They suggest that altering diet may have an impact on whether diabetes develops.

"Dietary interventions aimed at achieving or maintaining optimal butyrate-production levels might measurably reduce the risk of developing type 1 diabetes, especially in children with high-risk…genotypes," they conclude.

The authors have reported no relevant financial relationships.

Diabetologia. Published online June 12, 2014. Article

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