Our experimental results showed that SLBZP improved mitochondrial membrane permeability and the mitochondrial respiratory state of the liver cells of NAFLD mice, increased the mitochondrial OPR and ATP levels in the liver of NAFLD mice and regulated the UCP2/AMPK/IF1 signalling pathway, thereby affecting mitochondrial energy metabolism. Here, PRKAA1 is linked to metabolic dysfunction-associated steatotic liver disease.