<![CDATA[The global health burden of type 2 diabetes mellitus (T2DM) is growing, with over 537 million adults currently affected and a projected rise to 783 million by 2045. Despite the availability of pharmacological and lifestyle interventions, current therapies rarely reverse the underlying metabolic dysfunction, and most prior microbiome reviews have treated gut dysbiosis as a single undifferentiated phenomenon rather than distinguishing mechanistically distinct subtypes, which limits translation into targeted treatment. This review addresses that gap by synthesizing evidence from 83 original research studies sourced from PubMed, Scopus, Web of Science, and Embase (2015-2026). Gut microbiome dysbiosis is associated with insulin resistance through overlapping mechanisms, including disruption of intestinal barrier function by lipopolysaccharide (LPS)-driven endotoxemia and depletion of short-chain fatty acid (SCFA)-producing commensals such as Akkermansia muciniphila, Faecalibacterium prausnitzii, and Roseburia species. The meta-analysis reveals a substantial reduction in Akkermansia muciniphila abundance (Hedges’ g = -0.68, p = 0.002) and an overall HbA1c decrease of -0.72% (95% CI -1.12% to -0.32%) following synbiotic treatment. Building on this evidence, we propose a model that differentiates inflammatory-dominant from SCFA-depleted dysbiosis subtypes to guide targeted approaches such as probiotics, synbiotics, dietary fiber modulation, and fecal microbiota transplantation. In conclusion, the gut microbiome is a promising diagnostic biomarker and therapeutic target for T2DM, though subtype-stratified confirmatory trials are still needed.]]>
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