Impaired fatty acid oxidation and mitochondrial injury mediated by the AMPK/PPARα pathway: A key mechanism in high-fat diet-aggravated ulcerative colitis

Background

A high-fat diet (HFD) is closely associated with the progression of ulcerative colitis (UC). However, the underlying mechanisms, particularly the interplay among lipid metabolic disturbances, mitochondrial damage, and intestinal barrier dysfunction, remain poorly defined. This study aimed to elucidate the molecular mechanisms by which HFD exacerbates DSS-induced UC, with a focus on the role of the AMPK/PPARα axis in mediating lipotoxicity and mitochondrial dysfunction that promote UC progression.