PUBLICATION
Blockade of lipid accumulation by silibinin in adipocytes and zebrafish
- Authors
- Suh, H.J., Cho, S.Y., Kim, E.Y., Choi, H.
- ID
- ZDB-PUB-150107-7
- Date
- 2015
- Source
- Chemico-biological interactions 227: 53-62 (Journal)
- Registered Authors
- Keywords
- 3T3-L1, AMPKα, Adipogenesis, Cell cycle arrest, Silibinin, Zebrafish
- MeSH Terms
-
- 3T3-L1 Cells
- Adipocytes/cytology
- Adipocytes/drug effects
- Adipocytes/metabolism
- Adipogenesis/drug effects
- Animals
- Antioxidants/pharmacology*
- CCAAT-Enhancer-Binding Protein-alpha/genetics
- Cell Survival/drug effects
- Cyclin-Dependent Kinase Inhibitor p27/metabolism
- Embryo, Nonmammalian/drug effects
- Embryo, Nonmammalian/metabolism
- Fatty Acid-Binding Proteins/metabolism
- G1 Phase Cell Cycle Checkpoints/drug effects
- Kruppel-Like Transcription Factors/metabolism
- Larva/drug effects
- Larva/metabolism
- Lipid Metabolism/drug effects*
- Mice
- PPAR gamma/metabolism
- Signal Transduction/drug effects
- Silymarin/pharmacology*
- Zebrafish/growth & development
- PubMed
- 25559859 Full text @ Chem. Biol. Interact.
- CTD
- 25559859
Citation
Suh, H.J., Cho, S.Y., Kim, E.Y., Choi, H. (2015) Blockade of lipid accumulation by silibinin in adipocytes and zebrafish. Chemico-biological interactions. 227:53-62.
Abstract
Silibinin is a compound present mainly in milk thistle. In this study, we investigated the mechanism by which silibinin suppresses adipogenesis of 3T3-L1 cells, and evaluated the anti-adipogenic effect of silibinin in zebrafish. Silibinin reduced lipid accumulation by downregulating adipogenic factors, such as, peroxisome proliferator-activated receptor γ (PPARγ), CCAAT-enhancer binding protein α (C/EBPα), and fatty acid-binding protein 4 (FABP4). The reduction of these adipogenic protein levels was associated with the regulation of early adipogenic factors, such as, C/EBPβ and Krüppel-like factor 2 (KLF2), and was reflected in downregulation of lipid synthetic enzymes. Silibinin arrested cells in the G0/G1 phase of the cell cycle, accompanied by downregulation of cyclins and upregulation of p27, a cell cycle inhibitor. These results correlated with the finding of deactivation of extracellular signal-regulated kinase (ERK) and AKT, a serine/threonine-specific kinase. In addition, silibinin activated AMP-activated protein kinase α (AMPKα) to inhibit fatty acid synthesis. As observed in 3T3-L1 cells, silibinin inhibited lipid accumulation in zebrafish with the reduction of adipogenic factors and triglyceride levels. Our data revealed that silibinin inhibited lipid accumulation in 3T3-L1 cells and zebrafish, and this inhibitory effect was associated with abrogation of early adipogenesis via regulation of cell cycle and AMPKα signaling.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping