ME during pregnancy modulates offspring hepatic function via early hepatic programming while setting offspring hepatocytes into a “protective” metabolic state against the development of NAFLD by modulating five key mechanisms: I) decreased intrahepatic “de novo” lipogenesis via pAMPK and pACC, II) increased β-oxidation and mitochondrial biogenesis via PGC1α III) reduced intrahepatic triacylglycerol accumulation via pAMPK and PPARα IV) improved intrahepatic bile homeostasis via CYP7A1 and V) improved insulin resistance via SOCS3 (Fig. 8). Here, PPARGC1A is linked to Insulin resistance.