In the present study, we determined the effects of ME on hepatic key mechanisms of lipid and glucose homeostasis in offspring early life at programming peak (P21): on the molecular level we found indications for (I) decreased intrahepatic “de novo” lipogenesis, (II) increased β-oxidation and mitochondrial biogenesis, (III) improved intrahepatic bile homeostasis and (IV) improved hepatic insulin signaling, while offspring of exercised dams were protected against HFD-induced weight gain and NAFLD in later life (P112). The gene discussed is INS; the disease is metabolic dysfunction-associated steatotic liver disease.