Lipid (PA) stimulation induced AMPK phosphorylation and significantly increased the expression of PGC1α and its target, TFAM, along with OXPHOS and β oxidation genes in hepatocytes (Fig. 4D–F), suggesting that hepatocytes can activate oxidative metabolism pathways through the AMPK/PGC1α axis to respond to the excess lipid influx during MASLD. This evidence concerns the gene PPARGC1A and metabolic dysfunction-associated steatotic liver disease.