20 Jan Gut Inflammation & Bacterial Changes Linked to Type 1 Diabetes
MedicalResearch.com Interview with:
Prof Lorenzo Piemonti, MD
Professor of Endocrinology
Deputy Director, Diabetes Research Institute (SR-DRI)
Head, Beta Cell Biology Unit
Vita-Salute San Raffaele University,
San Raffaele Scientific Institute
MedicalResearch.com: What is the background for this study? What are the main findings?
Response: The potential role of gut inflammation and microbiome is becoming a hot topic in the field of diabetes. Several very recent publications report the presence of intestinal abnormalities associated with autoimmune diabetes in both experimental rodent models and patients. We have previously published that, compared to healthy subjects, patients with type 1 diabetes or at high risk of developing type 1 diabetes shows increased intestinal permeability.
Among the factors that may modify the intestinal barrier and impact on its immune activation, the gut microbiota is at present the main suspect. Our study is the first in literature that had the opportunity to analyze the inflammatory profile, the microbiome and their correlation on duodenum biopsies of patients with type 1 diabetes, in comparison with patients with celiac disease and healthy controls. Previous papers pointed out a significant difference in the composition of the stool microflora in subjects with autoimmune diabetes.
A major advancement of our work comes from the direct analysis of small intestine, instead of studies on stool samples. In fact, because of their close functional and spatial relationships, as well as a shared blood supply, it is logical to consider the duodenum and the pancreas correlated. We found big differences among the groups: gut mucosa in diabetes shows a peculiar signature of inflammation, a specific microbiome composition and we also discovered a strong association between some analysed inflammatory markers and specific bacteria genera. We think that our data add an important piece to disentangle the complex pathogenesis of type 1 diabetes and more generally of autoimmune diseases.
MedicalResearch.com: What should readers take away from your report?
Response: For years we have looked for the cause of type 1 diabetes in the pancreas; Perhaps we looked in the wrong place and there is the possibility that the intestines play a key role in the development of the disease
MedicalResearch.com: What recommendations do you have for future research as a result of this study?
Response: In our study the absence of correlation between inflammatory status and disease duration or glucose compensation suggest that chronic hyperglycemia is not causative of inflammation and could be a pathogenetic feature of the disease. It is however not possible to draw definitive conclusions about the correlation of these alterations with β cell autoimmunity, even if our driven hypothesis it is that the changes may be one of the causative factor for type 1 diabetes.
The next step is to study patients before type 1 diabetes onset. We know that it is possible to identify people at high risk of developing type 1 diabetes, in which the stigmata of autoimmunity are already present even if they have not yet clinical disease and the rise in blood sugar. Confirmation that the same alterations are present in this preclinical phase of the disease will strongly support the relationship with the autoimmunity and will open the possibility of new therapeutic approaches.
MedicalResearch.com: Is there anything else you would like to add?
Response: I want to thank all the patients who have made themselves available for this study knowing that they would not draw a personal benefit, but helped to increase our knowledge of the disease for the discovery of future therapies. No conflict of interest to disclosure
MedicalResearch.com: Thank you for your contribution to the MedicalResearch.com community.
Lorenzo Piemonti et al. Duodenal mucosa of patients with type 1 diabetes shows distinctive inflammatory profile and microbiota. Journal of Clinical Endocrinology & Metabolism, January 2017 DOI: 10.1210/jc.2016-3222
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