Fucosterol inhibits adipogenesis through the activation of AMPK and Wnt/β-catenin signaling pathways

Abstract

Fucosterol is a sterol constituent primarily derived from brown algae. Recently, the antiadipogenic effect of fucosterol has been reported; however, its molecular mechanism remains to be studied. Fucosterol effectively upregulated the phosphorylations of both adenosine monophosphate (AMP)-activated protein kinase (AMPK) and acetyl-CoA carboxylase (ACC), and downregulated the expression levels of lipogenesis-related factors. Moreover, fucosterol activated the major components of the Wnt/β-catenin signaling pathway, including β-catenin, disheveled 2 (DVL2), and cyclin D1 (CCND1), whereas it inactivated glycogen synthase kinase 3β (p-GSK3β) by stimulating its phosphorylation. In the presence or absence of fucosterol, the adipogenic transcriptional factors [peroxisome proliferator activated-receptor γ (PPARγ), CCAAT/enhancer binding protein α (C/EBPα), and sterol regulatory element binding protein-1c (SREBP-1c)] were upregulated by the inhibition of AMPK by compound C or the knockdown of β-catenin by siRNA. Overall, these data demonstrate that fucosterol prevents adipogenesis by mediating both AMPK- and Wnt/β-catenin-signaling pathways.