The role of the intestinal microbiota in type 1 diabetes mellitus

M Knip, H Siljander - Nature Reviews Endocrinology, 2016 - nature.com
M Knip, H Siljander
Nature Reviews Endocrinology, 2016nature.com
Type 1 diabetes mellitus (T1DM) is a chronic immune-mediated disease with a subclinical
prodromal period, characterized by selective loss of insulin-producing-β cells in the
pancreatic islets of genetically susceptible individuals. The incidence of T1DM has
increased several fold in most developed countries since World War II, in conjunction with
other immune-mediated diseases. Rapid environmental changes and modern lifestyles are
probably the driving factors that underlie this increase. These effects might be mediated by …
Abstract
Type 1 diabetes mellitus (T1DM) is a chronic immune-mediated disease with a subclinical prodromal period, characterized by selective loss of insulin-producing-β cells in the pancreatic islets of genetically susceptible individuals. The incidence of T1DM has increased several fold in most developed countries since World War II, in conjunction with other immune-mediated diseases. Rapid environmental changes and modern lifestyles are probably the driving factors that underlie this increase. These effects might be mediated by changes in the human microbiota, particularly the intestinal microbiota. Research on the gut microbiome of individuals at risk of developing T1DM and in patients with established disease is still in its infancy, but initial findings indicate that the intestinal microbiome of individuals with prediabetes or diabetes mellitus is different to that of healthy individuals. The gut microbiota in individuals with preclinical T1DM is characterized by Bacteroidetes dominating at the phylum level, a dearth of butyrate-producing bacteria, reduced bacterial and functional diversity and low community stability. However, these changes seem to emerge after the appearance of autoantibodies that are predictive of T1DM, which suggests that the intestinal microbiota might be involved in the progression from β-cell autoimmunity to clinical disease rather than in the initiation of the disease process.
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