Abstract
Type 1 diabetes (T1D) is the second most frequent autoimmune disease in childhood. The long-term micro- and macro-vascular complications of diabetes are associated with the leading causes of disability and even mortality in young adults. Understanding the T1D etiology will allow the design of preventive strategies to avoid or delay the T1D onset and to help to maintain control after developing. T1D development involves genetic and environmental factors, such as birth delivery mode, use of antibiotics, and diet. Gut microbiota could be the link between environmental factors, the development of autoimmunity, and T1D. In this review, we will focus on the dietary factor and its relationship with the gut microbiota in the complex process involved in autoimmunity and T1D. The molecular mechanisms involved will also be addressed, and finally, evidence-based strategies for potential primary and secondary prevention of T1D will be discussed.
Highlights
Type 1 diabetes (T1D) is one of the two most frequent autoimmune disorders in childhood and adolescence
The composition of the gut microbiota can be modulated by diet
This modulation can promote the proper maturation of the immune system, or, result in gut dysbiosis and aberrant immune responses that can lead to autoimmunity and T1D in predisposed children
Summary
Type 1 diabetes (T1D) is one of the two most frequent autoimmune disorders in childhood and adolescence. Since pancreatic β-cell autoimmunity appears frequently in the first 6 years of life, and its progression towards T1D can occur in preschoolers or during puberty, the factors investigated as possible triggers are related to early life and the immune system maturation process [5,6]. The gut microbiota could be the link between environmental factors and the development of autoimmunity and T1D. This has led to the proposal of a possible intestinal origin of T1D [9], and has placed the microbiota as the central factor for its study. The molecular mechanisms involved will be addressed, and evidence-based strategies for potential primary and secondary prevention of T1D will be discussed
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