In the present study, our results suggest a possible mechanism that may underlie NAFLD phenotypes in patients with IBD, which is related to main energy metabolic processes regulated via SIRT1/PGC-1α- and LXRα-mediated pathways by key metabolic regulators such as adiponectin, FGF21, and irisin. The gene discussed is PPARGC1A; the disease is metabolic dysfunction-associated steatotic liver disease.