LDLR and hyperlipidemia: Pretreatment with MO-A (10 mg/kg), a homoisoflavonoid, significantly ameliorated the hyperlipidemia in rats induced by high fat diet HFD through regulating the serum lipid profile by modulating the expression levels involved in lipogenesis and lipid oxidation, i.e., inducing the expression levels of both low-density lipoprotein receptor (LDLR) and peroxisome proliferators-activated receptors (PPAR) α, and suppressing the expression levels of both acetyl CoA carboxylase (ACC) and sterol regulatory element-binding protein 1c (SREBP-1C) (Li et al., 2020).