The results indicate that myricanol could be a potential therapeutic agent against obesity by activating the AMPK signaling pathway.

PMID: 

Food Chem. 2019 Jan 1 ;270:305-314. Epub 2018 Jul 18. PMID: 30174051

Abstract Title: 

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

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 theγ 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 adipogenesisand 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 suppressingadipogenic 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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