{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T23:47:55Z","timestamp":1792626475054,"version":"4.5.0"},"reference-count":100,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2025,11,17]],"date-time":"2025-11-17T00:00:00Z","timestamp":1763337600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Endocrinol."],"abstract":"<jats:p>Type 2 diabetes mellitus (T2DM) and metabolic dysfunction\u2013associated steatotic liver disease (MASLD) frequently co-occur and aggravate one another through shared pathways of insulin resistance, low-grade inflammation and disordered lipid handling. Framing their interaction through the gut\u2013liver\u2013pancreas axis, this review synthesizes recent progress with a function-first emphasis, moving beyond taxonomic lists to the microbial outputs most consistently linked to dual metabolic\u2013hepatic endpoints. We summarize how short-chain fatty acids (SCFAs), bile acids (BAs), lipopolysaccharide (LPS) and other microbe-associated molecular patterns, branched-chain amino-acid (BCAA) catabolites, trimethylamine N-oxide (TMAO) and endogenous ethanol reach the liver via portal inflow or the enterohepatic BA cycle and act on epithelial, immune and endocrine interfaces, including the farnesoid X receptor (FXR), G-protein\u2013coupled BA receptor 1 (TGR5) and fibroblast growth factor 19\/15 signaling. Mechanistic routes\u2014barrier dysfunction and endotoxaemia; SCFA signaling with effects on enteroendocrine tone and substrate flux; BA remodeling that resets hepatic and pancreatic set-points; and nitrogen\/choline and ethanol pathways that promote lipotoxic injury\u2014offer biologically coherent explanations for parallel trajectories of hyperglycemia and steatosis\/inflammation. We appraise therapeutic modulation spanning diet and fermentable substrates, live biotherapeutics\/postbiotics, BA-targeting drugs, fecal microbiota transplantation and metabolic\/bariatric surgery, and we outline clinically actionable biomarker opportunities using function-based panels (fermentative capacity, BA transformation, inflammatory ligands, nitrogen\/methyl flux) integrated with host metabolites and genetics for diagnosis, risk stratification and response prediction. By advocating standardized reporting, careful control of diet\/medications and composite metabolic\u2013hepatic endpoints in prospective trials, this review provides a practical framework to accelerate translation from association to targeted prevention and therapy that improves glycemic control and MASLD activity in parallel.<\/jats:p>","DOI":"10.3389\/fendo.2025.1677175","type":"journal-article","created":{"date-parts":[[2025,11,17]],"date-time":"2025-11-17T05:16:14Z","timestamp":1763356574000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":23,"title":["Microbiome\u2212mediated crosstalk between T2DM and MASLD: a translational review focused on 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