Here, using atherosclerosis-prone Seipin/Apoe dKO mice as a lipodystrophic mouse model, we showed that AT partially restored adipose function and markedly improved lipodystrophy-associated metabolic disorders, including hyperlipidemia, hepatic steatosis, and insulin resistance, followed by subsequently reduced atherosclerosis, although no significant improvement of PVAT abnormality or vascular dysfunction was observed. The gene discussed is APOE; the disease is fatty liver disease.