Saturday, October 28, 2017

Type I Diabetes: The Gut Microbiota Connection

By Mikael Häggström.When using this image in external works, it may be cited as:Häggström, Mikael (2014). "Medical gallery of Mikael Häggström 2014". WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.008. ISSN 2002-4436. Public Domain.orBy Mikael Häggström, used with permission. - See above. All used images are in public domain., Public Domain, https://commons.wikimedia.org/w/index.php?curid=6055517

The connection between gut microbiota and type 2 diabetes is known, and makes sense, as the long-term effects of the microbiota on the GI tract, food processing, secretion of factors inflammation, etc. can reasonably be seen as contributing to metabolic syndrome, insulin resistance, and, eventually, full-fledged type 2 diabetes. What is less well known is the link between intestinal bacteria and type 1 diabetes.  A review article has looked into this and concluded that two mechanisms may link the gut microbiota to type 1 diabetes.  First, if the infant has its GI tract colonized by sup-optimal bacteria, this will negatively affect the “education” of the immune system, resulting in a child vulnerable to immune system related diseases (e.g., autoimmune problems), including type 1 diabetes.  Note that type 1 diabetes results from autoimmune destruction if insulin-producing cells of the pancreases; therefore, an immune system not properly “trained” to distinguish “self” from “non-self” is “primed” to possibly result in attack against the targeted pancreatic cells.  Second, thus vulnerability, this predisposition, then develops into actual diabetes through the development of the antibodies that attack the pancreatic cells, and this development is associated with decreased diversity of the bacterial population of the gut, accompanied by an increase of certain bacterial species.  Protection against type 1 diabetes may therefore include modulating the colonization of the young intestinal tract to promote those bacterial species that would assist in normal immune function.  Abstract.


PURPOSE OF REVIEW:
The purpose of this review is to summarize potential modulations of the intestinal microbiome aimed at preventing or delaying progression to overt type 1 diabetes in the light of recently identified perturbations of the gut microbiota associated with the development of type 1 diabetes.
RECENT FINDINGS:
Accumulated data suggest that the gut microbiota is involved at two different steps in the evolution of type 1 diabetes. At the first step, the intestinal tract is colonized by a microbial community unable to provide an adequate education of the immune system. As a consequence, the infant acquires susceptibility to immune-mediated diseases, type 1 diabetes included. At the other step, the young child seroconverts to positivity for diabetes-associated autoantibodies. This is preceded or accompanied by a decrease in the diversity of the intestinal microbiota and an increased abundance of Bacteroides species. These changes will affect the disease process promoting progression toward overt type 1 diabetes. By providing specific probiotics, one can affect the colonization of the intestinal tract in the newborn infant or strengthen the immune education in early life. Human milk oligosaccharides function as nutrients for "healthy" bacteria. Dietary interventions applying modified starches can influence the numbers and activities of both autoreactive and regulatory T cells and provide protection against autoimmune diabetes in non-obese diabetic mice. Modulation of the intestinal microbiome holds the promise of effective protection against human type 1 diabetes.





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