LAUSR

Abstract Disclosure: L. Montejano: None. L.H. Graciolli: None. Y.S. Moura: None. A.J. Silva: None. G.D. Keller: None. B.S. Caxias: None. L.R. Prado: None. L.I. Silva: None. I.C. Mota: None. B.R. Pedrosa: None. M.C. Andrade: None. A.M. Santos: None. F.H. Santos: None. Introduction: Type 1 Diabetes Mellitus (T1D) is an autoimmune disease influenced by genetic, environmental, and gut microbiota factors. Despite evidence linking dysbiosis to autoimmunity, the specific mechanisms remain poorly understood. This study aims to identify microbial alterations in T1D, contributing to new prevention and management strategies. Materials and Methods: The systematic review was based on the PRISMA protocol. Searches were conducted in PubMed, Embase, and Cochrane to investigate whether intestinal dysbiosis could be correlated with the development of T1D in predisposed individuals. The search yielded 2,540 articles, and after deduplication and screening, seven studies were included in the final sample. Secondary, incomplete, duplicate studies and those without relevant outcomes were excluded. Results: Metagenomic sequencing of fecal samples consistently revealed reduced microbial diversity and specific taxonomic alterations, such as a decrease in Bifidobacterium species and a predominance of pro-inflammatory microorganisms. Additionally, functional analyses of the gut microbiota showed deficits in the production of short-chain fatty acids (SCFAs) and disruptions in pathways related to intestinal permeability and immune regulation. Intervention studies, such as the administration of Bifidobacterium infantis EVC001 in randomized clinical trials, demonstrated promising results in restoring microbial balance, reducing markers of intestinal inflammation, and potentially delaying autoimmune progression. Similarly, pilot studies using lactulose/mannitol intestinal permeability tests highlighted intestinal barrier dysfunction as an early biomarker of dysbiosis-induced autoimmunity. Moreover, research on children with HLA-conferred genetic risk factors showed that specific microbial profiles, including reduced butyrate-producing taxa, could stratify T1D risk even before the onset of autoimmunity. Conclusion: Despite advances in understanding the role of the gut microbiota in T1D, challenges persist, including variability in study designs, population heterogeneity, and a lack of longitudinal data. Future research should prioritize standardized protocols, larger sample sizes, and integrative approaches combining microbiome analysis with immunological and metabolic evaluations. These efforts are critical to advancing microbiota-targeted interventions as a viable strategy for T1D prevention and management. Presentation: Sunday, July 13, 2025