PUBLICATION

Myricanol mitigates lipid accumulation in 3T3-L1 adipocytes and high fat diet-fed zebrafish via activating AMP-activated protein kinase

Authors
Shen, S., Liao, Q., Feng, Y., Liu, J., Pan, R., Lee, S.M., Lin, L.
ID
ZDB-PUB-180904-1
Date
2019
Source
Food Chemistry   270: 305-314 (Journal)
Registered Authors
Keywords
AMP-activated protein kinase, Adipogenesis, Insulin sensitivity, Lipid accumulation, Myricanol, Zebrafish
MeSH Terms
  • 3T3-L1 Cells
  • AMP-Activated Protein Kinases/metabolism*
  • Adipocytes/cytology
  • Adipocytes/drug effects
  • Adipogenesis*/drug effects
  • Animals
  • CCAAT-Enhancer-Binding Protein-alpha
  • Diarylheptanoids/pharmacology*
  • Diet, High-Fat/adverse effects
  • Lipids
  • Mice
  • PPAR gamma
  • Zebrafish*
PubMed
30174051 Full text @ Food Chem.
Abstract
Myricanol is a diarylheptanoid isolated from Chinese bayberry. Through virtual docking strategy, myricanol was discovered as an AMP-activated protein kinase (AMPK) activator among a series of structural analogs, with high affinity for the γ subunit of AMPK. Myricanol was also evaluated for regulatory effects on lipid accumulation and insulin sensitivity in 3T3-L1 adipocytes and adiposity in high-fat diet-fed zebrafish. Myricanol suppressed lipid accumulation in 3T3-L1 cells in the initial stage (days 0-2) by suppressing adipogenesis and in the terminal stage (days 4-7) by inducing lipolysis and lipid combustion through activating AMPK. Moreover, myricanol enhanced insulin-stimulated glucose uptake by activating the insulin signaling pathway. In high-fat diet-fed zebrafish, myricanol inhibited lipid accumulation by suppressing adipogenic factors including peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT/enhancer binding protein α (C/EBPα). In summary, the results indicate that myricanol could be a potential therapeutic agent against obesity by activating the AMPK signaling pathway.
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