Butein inhibits adipocyte differentiation by modulating the AMPK pathway in 3T3-L1 cells

Butein (3,4,2',4'-tetrahydroxychalcone), a chalcone derivative, has been reported to exhibit various biological effects. However, the inhibitory effects of butein on adipocyte differentiation mediated via the adenosine 5'-monophosphate-activated protein kinase (AMPK) signaling pathway have not been investigated. This study elucidated the effects of butein treatment on adipogenesis regulated by the AMPK pathway using the 3T3-L1 cells. Butein inhibited lipid accumulation by regulating the early phase events of adipogenesis, and suppressed the expression of adipogenic transcription factors and their downstream target genes. Furthermore, AMPK and acetyl-CoA carboxylase (ACC) were significantly phosphorylated upon butein treatment in 3T3-L1 cells. The anti-adipogenic effects of butein were mediated by the activation of AMPK which was confirmed by using compound C, a highly specific inhibitor of AMPK. Butein also modulated enzymes involved in fatty acid metabolism such as ACC, carnitine palmitoyl transferase-1 (CPT-1), and glycerol-3-phosphate acyl transferase (GPAT)-1. Practical applicationsButein decreased lipid accumulation and adipocyte differentiation mediated via the AMPK signaling pathway in 3T3-L1 adipocytes. Based on these findings, it is suggested that butein may possess therapeutic potential for prevention and treatment of obesity and obesity-related diseases.