| Literature DB >> 27523648 |
James C Needell1, Danny Zipris2.
Abstract
The gastrointestinal system represents one of the largest interfaces between the human internal microenvironment and the external world. This system harbors trillions of commensal bacteria that reside in symbiosis with the host. Intestinal bacteria play a crucial role in maintaining systemic and intestinal immune and metabolic homeostasis because of their effect on nutrient absorption and immune development and function. Recently, altered gut bacterial composition (dysbiosis) was hypothesized to be involved in mechanisms through which islet autoimmunity is triggered. Evidence from animal models indicates that alterations in the gut bacterial composition precede disease onset, thus implicating a causal role for the gut microbiome in islet destruction. However, it remains unclear whether dysbiosis is directly linked to the mechanisms of human type 1 diabetes (T1D). In this review, we discuss data implicating the gut microbiota in disease progression with an emphasis on our recent studies performed in humans and in rodent models of T1D.Entities:
Keywords: 16S rRNA; Inflammation; Kilham rat virus; Microbiome; Type 1 diabetes
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Year: 2016 PMID: 27523648 DOI: 10.1007/s11892-016-0781-z
Source DB: PubMed Journal: Curr Diab Rep ISSN: 1534-4827 Impact factor: 4.810