Introduction: Type 2 diabetes is a complex endocrine-metabolic disorder in which insulin resistance, beta-cell dysfunction, chronic low-grade inflammation and environmental exposures interact. The gut microbiota has emerged as a biologically plausible determinant of this process because it regulates nutrient fermentation, microbial metabolite production, gut barrier integrity, immune tone and endocrine-metabolic signalling. Methods: A structured review of the literature was conducted using PubMed/MEDLINE, ScienceDirect and Google Scholar. English and French publications were screened using terms related to gut microbiota, type 2 diabetes, dysbiosis, insulin resistance, inflammation, probiotics, prebiotics, microbiota-targeted therapy and fecal microbiota transplantation. Forty-two records were identified, and 32 references were retained for qualitative synthesis after screening and full-text eligibility assessment. Results: The evidence consistently indicates that type 2 diabetes is associated with dysbiosis, reduced microbial diversity, depletion of butyrate-producing or metabolically favorable taxa and enrichment of opportunistic or pro-inflammatory communities. Recurrent mechanisms include intestinal barrier dysfunction, lipopolysaccharide-mediated metabolic endotoxemia, impaired short-chain fatty acid signalling, bile acid dysregulation, excessive imidazole propionate, branched-chain amino acid metabolism, altered incretin responses and immune-metabolic activation. Microbiota-targeted interventions, including fermented foods, probiotics, prebiotics, synbiotics, resistant starch and fecal microbiota transplantation, show promise but remain clinically heterogeneous. Conclusion: The gut microbiota is best understood as a dynamic metabolic interface rather than a passive marker of type 2 diabetes. Microbiome-informed strategies may enrich future precision endocrinology, but standardised human trials integrating taxonomic, functional and clinical endpoints are required before routine implementation.