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MinnesotaMicrobiome Changed by Gluten Increases Incidences of Type 1 Diabetes, say Mayo Clinic Researchers
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ROCHESTER, Minn. — Research has shown that the intestinal microbiome plays a large role in the development of Type 1 diabetes. Now, researchers at Mayo Clinic have demonstrated that gluten in the diet may modify the intestinal microbiome, increasing incidences of Type 1 diabetes. The research was published Nov. 13, in the journal PLOS ONE.
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These researchers demonstrated that mice fed a gluten-free diet had a dramatically reduced incidence of Type 1 diabetes. These mice were non-obese diabetic mice, or mice that grow to develop Type 1 diabetes. The gluten-free diet worked to protect the mice against Type 1 diabetes. When the researchers added gluten back into the diets of mice it reversed the protective effect the gluten free diet had provided. There also was a measurable impact of the gluten on the bacterial flora of the mice that might be one way in which gluten could affect the risk for diabetes.
"These changes suggest that the presence of gluten is directly responsible for the diabetes-creating effects of diet and determines the gut microflora," says Govindarajan Rajagopalan, Ph.D., a Mayo Clinic immunologist and study author.
Researchers point out that this research suggests dietary interventions may be crucially important in affecting the likelihood of the development of Type 1 diabetes. "While this is purely an animal-based study, it allows us to manipulate these mice in such a way as to study the effects of certain diets, and these diet changes seem to make an impact on the likelihood of developing the mouse equivalent of type 1 diabetes," says Joseph Murray, M.D., a Mayo Clinic gastroenterologist and study author.
The next step for these researchers is similar studies in humans. A study is starting at Mayo Clinic for newly-diagnosed Type 1 diabetic patients. Information about the study is available at ClinicalTrials.gov.
The study was funded by the Iacocca Foundation and a National Institutes of Health RO1 grant.
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