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 language | English |
|---|---|
| Pages (from-to) | 489-494 |
| Number of pages | 6 |
| Journal | Food Science and Biotechnology |
| Volume | 26 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 2017 Apr 1 |
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All Science Journal Classification (ASJC) codes
- Biotechnology
- Food Science
- Applied Microbiology and Biotechnology
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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 journal › Article
TY - JOUR
T1 - Fucosterol inhibits adipogenesis through the activation of AMPK and Wnt/β-catenin signaling pathways
AU - Song, Youngwoo
AU - Oh, Ga Hui
AU - Kim, Mi Bo
AU - Hwang, Jae-Kwan
PY - 2017/4/1
Y1 - 2017/4/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85018504858&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85018504858&partnerID=8YFLogxK
U2 - 10.1007/s10068-017-0067-5
DO - 10.1007/s10068-017-0067-5
M3 - Article
AN - SCOPUS:85018504858
VL - 26
SP - 489
EP - 494
JO - Food Science and Biotechnology
JF - Food Science and Biotechnology
SN - 1226-7708
IS - 2
ER -