Premium
Seanol® and its major compound, dieckol suppress lipid accumulation during adipogenesis through inhibition of Mitotic Clonal Expansion (MCE) and cell cycle arrest.
Author(s) -
Choi HyeonSon,
Jeon HuiJeon,
Lee OkHwan,
Lee BooYong
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.1079.29
Subject(s) - adipogenesis , 3t3 l1 , lipid droplet , adipocyte , oil red o , chemistry , downregulation and upregulation , microbiology and biotechnology , biology , biochemistry , adipose tissue , gene
Seanol ® is a polyphenol extract derived from a brown alga, Ecklonia cava (EC), which is native to the sea off Korea and Japan. It consists of phlorotannins including eckol and dieckol. In this study, we investigated the effect of Seanol ® and its major compounds, eckol and dieckol on adipocyte differentiation in 3T3‐ L1 cells. Our data showed that Seanol ® and dieckol inhibited lipid accumulation in 3T3‐L1 in a dose dependent manner, while eckol didn't have a significant inhibitory effect on lipid accumulation in Oil red O staining, suggesting that dieckol plays as a major inhibitory compound of Seanol ® on lipid accumulation. The inhibition of dieckol was usually occurred in early stage of adipogenesis. Dieckol inhibited mRNA expression of early adipogenic genes such as CCAAT/ enhancer binding protein‐β (C/EBPβ), C/EBPδ, Krueppel‐like factor 4 (KLF4), and KLF5, whereas it enhanced mRNA expression of preadipocyte secreted factor (Pref‐1) in RT‐PCR. These results were reflected in downregulation of late adipogenic factors such as peroxisome proliferator‐activated receptor‐γ (PPARγ), C/EBPα, and adipocyte protein 2 (ap2). Our cell cycle analysis showed that dieckol inhibited MCE stage through the arrest of G1/G0 phase, which is supported by suppression of adipocyte proliferation in trypan blue assay. Our study suggests that dieckol is a potential edible agent in controlling lipid accumulation in metabolic disorder.