Gut dysbiosis in PMOS: link to MASLD and role of synbiotics

AbstractPolyendocrine metabolic ovarian syndrome (PMOS), previously termed Polycysticovary syndrome (PCOS), is a multifactorial endocrine and metabolic disordercharacterized by hyperandrogenism, ovulatory dysfunction, insulin resistance, obesity,chronic low-grade inflammation, and metabolic abnormalities. Emerging evidenceindicates that gut microbiota dysbiosis plays a central role in the development andprogression of PMOS through mechanisms involving endotoxemia, altered short-chainfatty acid production, intestinal permeability, inflammatory signaling, and metabolicdysfunction. Dysbiosis-induced activation of the gut–liver axis contributes significantlyto hepatic steatosis and progression toward metabolic dysfunction-associated steatoticliver disease (MASLD) and metabolic dysfunction-associated steatohepatitis (MASH).Altered microbial metabolites, bile acid dysregulation, and activation of inflammatorypathways including Toll-like receptor-4 and nuclear factor-kappa B further aggravateinsulin resistance and ovarian dysfunction. Recent experimental and clinical studieshave demonstrated beneficial effects of probiotics, prebiotics, synbiotics, and fecalmicrobiota transplantation in restoring gut microbial balance and improving endocrineand metabolic abnormalities associated with PMOS. This review summarizes currentevidence regarding the role of gut dysbiosis in PMOS, mechanisms linking PMOS withMASLD/MASH, gut–liver axis dysfunction, and the therapeutic potential ofmicrobiota-targeted interventions.