Fatty acid oxidation and inflammatory bowel disease: Highlighting the roles of pathogenesis and treatment.

The increasing prevalence of inflammatory bowel disease (IBD) imposes a substantial economic burden, and its pathogenesis is associated with dietary fat intake. Short-chain fatty acids (SCFAs) regulate intestinal inflammation and immunity by inhibiting histone deacetylases (HDACs) or binding to G protein-coupled receptors (GPCRs). Specialized pro-resolving mediators (SPMs) derived from polyunsaturated fatty acids (PUFAs) contribute to inflammation resolution. Fatty acid oxidation (FAO) is a primary energy source for intestinal epithelial cells. Previous studies indicate that patients with IBD exhibit decreased levels of SCFAs and reduced intermediates of the tricarboxylic acid (TCA) cycle, suggesting impaired FAO. These alterations may exacerbate intestinal inflammation through energy deficiency in intestinal epithelial cells, barrier disruption, and dysregulated immune cell polarization. This review aims to broaden therapeutic options by identifying underlying targets and proposing potential strategies.