摘要The prevalence of metabolic dysfunction-associated steatotic liver disease(MASLD)is higher among individuals with inflammatory bowel disease(IBD)than in the general population.Emerging evidence indicates that the development of MASLD in patients with IBD may occur independently of traditional metabolic risk factors,suggesting a unique pathophysiological mechanism distinct from conventional MASLD pathways.Bile acids(BAs),which act as critical signaling molecules in enterohepatic circulation,play an essential role in maintaining gastrointestinal homeostasis through bidirectional gut-liver axis communication.These molecules are increasingly recognized as pivotal regulators in the progression of both MASLD and IBD.While previous studies have characterized the dynamics of BA in blood or fecal samples under both conditions,a comprehensive understanding of their metabolic profiles and the associated interactions within the gut-liver axis is still lacking.This review synthesizes current evidence from studies employing BA metabolomics to investigate IBD and MASLD.By focusing on BA signatures,we summarize conserved alterations between these two conditions and their potential mechanisms of disease progression.Our review advances understanding of BA-mediated pathways in IBD and MASLD,providing a foundation for assessing their roles in contributing to the pathogenesis of MASLD in patients with IBD.