Table 1 provides a comparative overview of microbiota-based interventions in diabetes, emphasizing their underlying mechanisms and reported effects on β-cell function. Figure 2B focuses on direct and incretin-mediated signaling to the β-cell, depicting how BefA, LPS and microbial tryptophan metabolites act on intestinal epithelial and enteroendocrine cells to modulate GIP and GLP-1 secretion and how these hormones, together with BefA, engage GIPR/GLP1R, cAMP–PKA/EPAC2 and PI3K/AKT pathways to regulate β-cell Ca2+ influx, survival, proliferation and insulin granule exocytosis. This evidence concerns the gene INS and diabetes mellitus.