Editors' ChoiceDiabetes

Microbes and Type 1 Diabetes

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Science Translational Medicine  16 Jan 2013:
Vol. 5, Issue 168, pp. 168ec14
DOI: 10.1126/scitranslmed.3005668

Type 1 diabetes (T1D) is caused by the destruction of pancreatic β-cells (which produce insulin) by T cells, although the exact steps of T1D disease progression are not fully understood. Now, de Goffau et al. have uncovered an immunological link between the pancreas and gastrointestinal tract that may contribute to T1D development.

There are roughly 100 trillion microorganisms within the human intestine that are involved in regulating the gut’s immune system, specifically the T cells. The authors hypothesized that there were differences in the composition of intestinal microbiota in autoantibody-negative children and children with at least two diabetes-associated autoantibodies (“autoantibody-positive” children, who are prone to develop T1D). The subjects were matched for age, sex, histocompatibility locus antigen (HLA) risk genotype, and early feeding history. Using principal component analysis at the species level, the authors found that there was a low abundance of lactate- and butyrate-producing bacteria—including two of the most common bifidobacteria—in the autoantibody-positive children, which suggests that these bacteria are associated with β-cell autoimmunity. In addition, the number of β-cell autoantibodies was inversely correlated with levels of butyrate-producing bacterium. These data imply that the number of autoantibodies in children—and, hence, T1D—may be affected by changes in the gut bacterial population.

Butyrate may have beneficial impacts on gut biology. Although there were no differences in fecal calprotectin or immunoglobulin A levels (biological markers of gut inflammation), de Goffau and colleagues suggest that butyrate levels may be critical in the regulation of autoreactive T cells during the development of T1D. Future studies will be needed to determine whether fecal microbiota involved in butyrate production pathways can prevent β-cell autoimmunity. Such findings would suggest that alterations in intestinal bacterial diversity in favor of butyrate-producing species may be an effective therapeutic strategy for T1D.

M. C. de Goffau et al., Fecal microbiota composition differs between children with β-cell autoimmunity and those without. Diabetes, published online 28 December 2012 (10.2337/db12-0526). [PubMed]

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