Collectively, this study reveals that the molecular mechanisms behind RRBE’s ability to alleviate hepatosteatosis and hyperlipidemia in the HFD mouse model are likely associated with the balanced expression of major genes involved in adipose tissue lipolysis (ATGL), hepatic FA uptake (CD36), hepatic FA and TG synthesis (LXRα and SREBP-1c), hepatic FA oxidation (CPT1A), hepatic cholesterol synthesis (SREBP-2 and HMGCR), and circulating TG degradation (LPL). The gene discussed is SREBF1; the disease is hyperlipidemia.