Licochalcone A prevents adipocyte differentiation and lipogenesis via suppression of peroxisome proliferator-activated receptor γ and sterol regulatory element-binding protein pathways.

Licochalcone A (LA) has been shown to exert multiple pharmacological effects, including anti-inflammatory, antiparasitic, antifungal, anticancer, and osteogenic activities. The present study investigated the ability of LA to suppress the differentiation of 3T3-L1 preadipocytes, and its antiobesity activity was explored using high fat diet (HFD)-fed ICR mice. During the terminal differentiation process, 3T3-L1 preadipocytes were treated with LA, and the lipid contents were quantified along with any changes in the expression of biomarkers associated with adipocyte differentiation and lipogenesis. The results show that LA significantly reduced lipid accumulation and down-regulated the expression of peroxisome proliferator-activated receptor γ, CCAAT/enhancer binding protein α, sterol regulatory element-binding protein 1c, and their target genes (fatty acid binding protein, fatty acid synthase, stearoyl-CoA desaturase 1, and glycerol-3-phosphate acyltransferase). In an animal study, body weight, triglyceride, cholesterol, and nonesterified fatty acid levels in the group given 10 mg/kg LA were significantly decreased by 14.0, 48.2, 58.9, and 73.5%, respectively. Transverse microcomputed tomography indicated that visceral fat depots in LA-treated mice were markedly reduced when compared with those of the HFD control group. In summary, these results suggest that LA exerts an antiobesity effect and that it is a candidate for future clinical trials.