PUBLICATION
Cholecalciferol inhibits lipid accumulation by regulating early adipogenesis in cultured adipocytes and zebrafish
- Authors
- Kim, J.H., Kang, S., Jung, Y.N., Choi, H.S.
- ID
- ZDB-PUB-151226-3
- Date
- 2016
- Source
- Biochemical and Biophysical Research Communications 469(3): 646-53 (Journal)
- Registered Authors
- Keywords
- 3T3-L1, AMPKα, adipogenesis, cell cycle arrest, cholecalciferol, zebrafish
- MeSH Terms
-
- Adipocytes/cytology*
- Adipocytes/drug effects
- Adipocytes/metabolism*
- Adipogenesis/drug effects
- Adipogenesis/physiology*
- Animals
- Cell Cycle Checkpoints/drug effects
- Cell Cycle Checkpoints/physiology
- Cells, Cultured
- Cholecalciferol/administration & dosage*
- Dose-Response Relationship, Drug
- Gene Expression Regulation, Developmental/drug effects
- Gene Expression Regulation, Developmental/physiology
- Lipid Metabolism/drug effects
- Lipid Metabolism/physiology*
- Zebrafish/anatomy & histology
- Zebrafish/physiology
- PubMed
- 26703207 Full text @ Biochem. Biophys. Res. Commun.
Citation
Kim, J.H., Kang, S., Jung, Y.N., Choi, H.S. (2016) Cholecalciferol inhibits lipid accumulation by regulating early adipogenesis in cultured adipocytes and zebrafish. Biochemical and Biophysical Research Communications. 469(3):646-53.
Abstract
Cholecalciferol (CCF) is a common dietary supplement as a precursor of active vitamin D. In the present study, the effect of CCF on lipid accumulation was investigated in adipocyte cells and zebrafish models. CCF effectively inhibited lipid accumulation in both experimental models; this effect was attributed to the CCF-mediated regulation of early adipogenic factors. CCF down-regulated the expressions of CCAAT-enhancer-binding protein-β (C/EBPβ), C/EBPδ, Krueppel-like factor (KLF) 4, and KLF5, while KLF2, a negative adipogenic regulator, was increased by CCF treatment. CCF inhibited cell cycle progression of adipocytes through down-regulation of cyclin A and cyclinD; p-Rb was suppressed by CCF, but p27 was up-regulated with CCF treatment. This CCF-mediated inhibition of cell cycle progression is highly correlated to the inhibitions of extracellular signal-regulated kinase (ERK), serine threonine-specific kinase (AKT), and mammalian target of rapamycin (mTOR). Furthermore, CCF-induced inactivation of acetyl-CoA carboxylase (ACC), a fatty acid synthetic enzyme, with the activation of AMP-activated protein kinase α (AMPKα) was also observed. Consistent with the observations in adipocytes, CCF effectively inhibited lipid accumulation with the down-regulation of adipogenic factors in zebrafish. The present study indicates that CCF showed anti-adipogenic effect in adipocytes and zebrafish, and its inhibitory effect was involved in the regulation of early adipogenic events including cell cycle arrest and activation of AMPKα signaling.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping