Type 1 Diabetes (T1D) is regarded as an autoimmune disease characterized by insulin deficiency resulting from destruction of pancreatic β-cells. The incidence rates of T1D have increased worldwide. Over the past decades, progress has been made in understanding the complexity of the immune response and its role in T1D pathogenesis, however, the trigger of T1D autoimmunity remains unclear. The increasing incidence rates, immigrant studies, and twin studies suggest that environmental factors play an important role and the trigger cannot simply be explained by genetic predisposition. Several research initiatives have identified environmental factors that potentially contribute to the onset of T1D autoimmunity and the progression of disease in children/young adults. More recently, the interplay between gut microbiota and the immune system has been implicated as an important factor in T1D pathogenesis. Although results often vary between studies, broad compositional and diversity patterns have emerged from both longitudinal and cross-sectional human studies. T1D patients have a less diverse gut microbiota, an increased prevalence of Bacteriodetes taxa and an aberrant metabolomic profile compared to healthy controls. In this comprehensive review, we present the data obtained from both animal and human studies focusing on the large longitudinal human studies. These studies are particularly valuable in elucidating the environmental factors that lead to aberrant gut microbiota composition and potentially contribute to T1D. We also discuss how environmental factors, such as birth mode, diet, and antibiotic use modulate gut microbiota and how this potentially contributes to T1D. In the final section, we focus on existing recent literature on microbiota-produced metabolites, proteins, and gut virome function as potential protectants or triggers of T1D onset. Overall, current results indicate that higher levels of diversity along with the presence of beneficial microbes and the resulting microbial-produced metabolites can act as protectors against T1D onset. However, the specifics of the interplay between host and microbes are yet to be discovered.
It seems that type 1 diabetes responds to an autoimmune response of the organism, one of the possible causes being the reaction to the intestinal flora present in the human intestine.
Type 1 diabetes, previously called juvenile diabetes, consists of a destruction of the pancreatic islets (Langerhans), responsible for the production of insulin.
Several studies point to the fact that an immune reaction of the body itself could trigger the attack on pancreatic cells and produce type 1 diabetes. Bacteria present in the intestine could be one of the triggers of type 1 diabetes, by generating an immune response that would be harmful to the body.
Enteric bacteria belong to other species, they are prokaryotic cells, which have a symbiotic relationship with the human organism, taking advantage of nutrients from the digestive system and contributing to intestinal function. However, they are still foreign organisms, to which the body responds with defensive actions.