Mechanistic studies revealed that PA alleviated lipid accumulation in HFD-induced NAFLD by activating the phosphorylation of AMPKα and ACC, inhibiting the expression of SREBF1 and FASN to reduce hepatic lipogenesis, and increasing the expression of ATGL, PPARα, and PPARγ to promote lipolysis and fatty acid oxidation. The gene discussed is SREBF1; the disease is metabolic dysfunction-associated steatotic liver disease.