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

Youngwoo Song, Ga Hui Oh, Mi Bo Kim, Jae-Kwan Hwang

Research output: Contribution to journalArticle

4 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)489-494
Number of pages6
JournalFood Science and Biotechnology
Volume26
Issue number2
DOIs
Publication statusPublished - 2017 Apr 1

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Catenins
AMP-activated protein kinase
Adipogenesis
Wnt Signaling Pathway
AMP-Activated Protein Kinases
sterols
binding proteins
phosphorylation
acetyl-CoA carboxylase
Phaeophyceae
lipogenesis
cyclins
small interfering RNA
transcription factors
Phosphorylation
Sterol Regulatory Element Binding Protein 1
CCAAT-Enhancer-Binding Proteins
Phaeophyta
Glycogen Synthase Kinase 3
Acetyl-CoA Carboxylase

All Science Journal Classification (ASJC) codes

  • Biotechnology
  • Food Science
  • Applied Microbiology and Biotechnology

Cite this

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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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Fucosterol inhibits adipogenesis through the activation of AMPK and Wnt/β-catenin signaling pathways. / Song, Youngwoo; Oh, Ga Hui; Kim, Mi Bo; Hwang, Jae-Kwan.

In: Food Science and Biotechnology, Vol. 26, No. 2, 01.04.2017, p. 489-494.

Research output: Contribution to journalArticle

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