From gut to liver: Exploring the relationship between inflammatory bowel disease and metabolic dysfunction-associated steatotic liver disease

Inflammatory bowel disease (IBD), comprising Crohn's disease and ulcerative colitis, is a chronic condition marked by relapsing inflammation of the gastrointestinal tract. Metabolic dysfunction-associated steatotic liver disease (MASLD) emphasizes the interplay between metabolic alterations and modern lifestyle factors in its pathogenesis. Emerging evidence suggests that individuals with IBD are at increased risk for MASLD, driven by shared mechanisms, including gut dysbiosis, chronic systemic inflammation, and compromised intestinal barrier function. However, MASLD frequently remains underdiagnosed in this population. The gut microbiota plays a central role in modulating these interactions, influencing both intestinal permeability and metabolic regulation. Key pathophysiological mechanisms include alterations in short-chain fatty acid production, particularly reduced butyrate synthesis; disruption of bile acid signaling pathways <i>via</i> farnesoid X receptor and Takeda G protein-coupled receptor 5 receptors; and activation of pro-inflammatory cascades through toll-like receptor 4 in the liver. These events lead to increased intestinal permeability, translocation of microbial products, and amplification of hepatic inflammation. This review synthesizes current knowledge on the shared pathophysiological pathways linking IBD and MASLD-focusing on dysbiosis, barrier dysfunction, and inflammation-and underscores their clinical relevance. Understanding the gut-liver axis provides opportunities for early diagnosis and integrated management strategies, aiming to reduce disease burden and improve patient outcomes.