This review comprehensively examines the role and mechanisms of Urolithin A (UroA), a gut microbial metabolite derived from dietary ellagitannins (ETs), in ameliorating obesity and related metabolic disorders. The in vivo production of UroA is strictly dependent on specific gut microbiota, and the substantial inter-individual variation in this metabolic capacity (UM phenotype) directly influences population responsiveness to ETs-rich dietary interventions. Mechanistically, UroA acts through multiple coordinated pathways: it activates thermogenesis in brown and beige adipose tissue to promote energy expenditure; bidirectionally regulates lipid metabolism by enhancing fatty acid oxidation while suppressing lipogenesis; remodels the immune microenvironment by polarizing macrophages toward the anti-inflammatory M2-like phenotype to alleviate chronic inflammation; and modulates gut microbiota composition at multiple taxonomic levels and regulates microbial tryptophan metabolism, alongside enhancing intestinal barrier integrity. These integrated effects collectively improve systemic insulin sensitivity, glucose homeostasis, and reduce lipid accumulation. Although preclinical evidence is robust, its efficacy in humans requires further validation through large-scale clinical trials. In summary, UroA represents a pivotal active molecule within the “diet-microbiota-host” interaction axis, offering a novel scientific rationale and a potential target for developing personalized nutritional strategies against obesity and other metabolic diseases.

Background: Ulcerative colitis (UC) is a chronic relapsing inflammatory bowel disease. Intestinal barrier impairment represents a core pathogenic mechanism and a key therapeutic target for achieving mucosal healing and sustained remission. Methods: This narrative review summarizes intestinal barrier structure, disruption mechanisms, barrier-targeted therapies, and non-invasive monitoring approaches. A reproducible literature search was conducted in PubMed, Web of Science, and ClinicalTrials.gov from 2015 to 2026. Results: Barrier disruption in UC involves genetic susceptibility, proinflammatory cytokines, zonulin-mediated tight junction injury, gut microbiota dysbiosis, decreased short-chain fatty acids and secondary bile acids, impaired autophagy, and an abnormal mucin 2 (MUC2)-dependent mucus layer. Validated non-invasive monitoring tools include fecal calprotectin/lactoferrin, intestinal ultrasound, diffusion-weighted magnetic resonance imaging (MRI), and intravoxel incoherent motion (IVIM). Emerging therapies focus on tight junction stabilization, epithelial regeneration, autophagy regulation, MUC2 restoration, and microbiota modulation. Conclusions: Intestinal barrier dysfunction drives the initiation and progression of UC. Barrier-based monitoring and targeted repair strategies improve UC management. Future studies should develop personalized therapies, precise microbiota engineering, and multi-dimensional digital evaluation systems.

Ulcerative colitis (UC) is a chronic, relapsing-remitting subtype of inflammatory bowel disease (IBD), featured by continuous mucosal inflammation restricted to the colon and rectum. Although the exact pathogenesis of UC has not been fully clarified, intestinal barrier impairment and disrupted mucosal homeostasis are recognized as the central mechanism. Therefore, restoring intestinal mucosal barrier function represents a core strategy for UC prevention and treatment, which aligns with the therapeutic goal of achieving mucosal healing and sustained remission. In this review, we outline the composition and functional significance of the intestinal barrier, explore key mechanisms underlying its disruption, and summarize recent advances in UC-related monitoring strategies. Finally, we explore novel therapeutic approaches aimed at epithelial barrier repair. The review aims to provide insights valuable for both basic research and clinical management of UC.