The GLP-1–Gut Microbiota–Autoimmunity Axis in Type 1 Diabetes: Emerging Evidence and Mechanistic Perspectives

Type 1 diabetes (T1D) is an autoimmune disease in which genetic susceptibility interacts with environmental and immunometabolic factors. Growing evidence implicates gut dysbiosis, impaired intestinal barrier integrity, and altered microbial metabolites in the loss of immune tolerance and β-cell autoimmunity. Microbiota-derived metabolites regulate enteroendocrine glucagon-like peptide-1 (GLP-1) secretion, epithelial barrier function, and immune responses. Conversely, GLP-1 signaling and incretin-based therapies may modify the intestinal environment and microbial composition. Overall, the GLP-1–gut microbiota axis is a promising therapeutic target. Activation of the GLP-1 receptor suppresses pro-inflammatory pathways while promoting anti-inflammatory ones; all these effects may protect β-cells. Caveolin-1 may represent a molecular hub linking the GLP-1–gut microbiota–autoimmunity axis in T1D. This narrative review examines the bidirectional relationship between GLP-1 signaling and the gut microbiota and its potential relevance to T1D.