PUBLICATION
Seapolynol Extracted from Ecklonia cava Inhibits Adipocyte Differentiation in Vitro and Decreases Fat Accumulation in Vivo
- Authors
- Jeon, H.J., Choi, H.S., Lee, Y.J., Hwang, J.H., Lee, O.H., Seo, M.J., Kim, K.J., Lee, B.Y.
- ID
- ZDB-PUB-151223-7
- Date
- 2015
- Source
- Molecules 20: 21715-31 (Journal)
- Registered Authors
- Keywords
- 3T3-L1, ICR mouse, adipogenesis, seapolynol, zebrafish
- MeSH Terms
-
- 3T3-L1 Cells
- Adipocytes/drug effects
- Adipocytes/physiology*
- Adipogenesis/drug effects
- Adiposity
- Animals
- Anti-Obesity Agents/isolation & purification
- Anti-Obesity Agents/pharmacology*
- Anti-Obesity Agents/therapeutic use
- Cell Differentiation/drug effects*
- Cell Proliferation/drug effects
- Diet, High-Fat/adverse effects
- Lipid Metabolism/drug effects*
- Male
- Mice
- Mice, Inbred ICR
- Mitosis/drug effects
- Obesity/drug therapy
- Phaeophyceae/chemistry
- Polyphenols/isolation & purification
- Polyphenols/pharmacology*
- Polyphenols/therapeutic use
- Signal Transduction
- Zebrafish
- PubMed
- 26690099 Full text @ Molecules
Citation
Jeon, H.J., Choi, H.S., Lee, Y.J., Hwang, J.H., Lee, O.H., Seo, M.J., Kim, K.J., Lee, B.Y. (2015) Seapolynol Extracted from Ecklonia cava Inhibits Adipocyte Differentiation in Vitro and Decreases Fat Accumulation in Vivo. Molecules. 20:21715-31.
Abstract
Seapolynol (SN) is a polyphenol mixture derived from Ecklonia cava. We evaluated the effects of SN on lipid accumulation in adipocytes, zebrafish, and mice. SN effectively inhibited lipid accumulation in three experimental models by suppressing adipogenic factors. Triglyceride synthetic enzymes such as diacylglycerol acyltransferase 1 (DGAT1) and GPAT3 were also downregulated by SN. This SN-induced inhibition of adipogenic factors was shown to be due to the regulatory effect of SN on early adipogenic factors; SN downregulated the expression of Krueppel-like factor 4 (KLF4), KLF5, CCAAT-enhancer-binding protein β (C/EBPβ), C/EBPδ, and Protein C-ets-2 (ETS2), while KLF2, an anti-early adipogenic factor, was upregulated by SN. SN-mediated inhibition in early adipogenesis was closely correlated with the inhibition of mitotic clonal expansion via cell cycle arrest. SN inhibited cell cycle progression by suppressing cell cycle regulators, such as cyclin A, cyclinD, and pRb but increased p27, a cell cycle inhibitor. In a mouse study, SN effectively reduced body weight and plasma lipid increases induced by a high-fat diet; triglycerides, total cholesterol, and low-density lipoprotein (LDL) levels were markedly reduced by SN. Moreover, SN remarkably improved high-fat-diet-induced hepatic lipid accumulation. Furthermore, SN activated AMP-activated protein kinase-α (AMPKα), an energy sensor, to suppress acetyl-coA carboxylase (ACC), inhibiting lipid synthesis. Our study suggests that SN may be an edible agent that can play a positive role in prevention of metabolic disorders.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping