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

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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.

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Correspondence to Jae-Kwan Hwang.

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Song, Y., Oh, G.H., Kim, MB. et al. Fucosterol inhibits adipogenesis through the activation of AMPK and Wnt/β-catenin signaling pathways. Food Sci Biotechnol 26, 489–494 (2017). https://doi.org/10.1007/s10068-017-0067-5

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  • DOI: https://doi.org/10.1007/s10068-017-0067-5

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