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Phillyrin attenuates high glucose-induced lipid accumulation in human HepG2 hepatocytes through the activation of LKB1/AMP-activated protein kinase-dependent signalling.

Abstract
Phillyrin, an active constituent found in many medicinal plants and certain functional foods, has anti-obesity activity in vivo. The aim of our study was to provide new data on the molecular mechanism(s) underlying the role of phillyrin in the prevention of high glucose-induced lipid accumulation in human HepG2 hepatocytes. We found that phillyrin suppressed high glucose-induced lipid accumulation in HepG2 cells. Phillyrin strongly inhibited high glucose-induced fatty acid synthase (FAS) expression by modulating sterol regulatory element-binding protein-1c (SREBP-1c) activation. Moreover, use of the pharmacological AMP-activated protein kinase (AMPK) inhibitor compound C revealed that AMPK is essential for suppressing SREBP-1c expression in phillyrin-treated cells. Finally, we found that liver kinase B1 (LKB1) phosphorylation is required for the phillyrin-enhanced activation of AMPK in HepG2 hepatocytes. These results indicate that phillyrin prevents lipid accumulation in HepG2 cells by blocking the expression of SREBP-1c and FAS through LKB1/AMPK activation, suggesting that phillyrin is a novel AMPK activator with a role in the prevention and treatment of obesity.
AuthorsMinh Truong Do, Hyung Gyun Kim, Jae Ho Choi, Tilak Khanal, Bong Hwan Park, Thu Phuong Tran, Yong Pil Hwang, Minkyun Na, Hye Gwang Jeong
JournalFood chemistry (Food Chem) Vol. 136 Issue 2 Pg. 415-25 (Jan 15 2013) ISSN: 1873-7072 [Electronic] England
PMID23122079 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2012 Elsevier Ltd. All rights reserved.
Chemical References
  • Glucosides
  • Plant Extracts
  • Protein Serine-Threonine Kinases
  • STK11 protein, human
  • AMP-Activated Protein Kinase Kinases
  • AMP-Activated Protein Kinases
  • Glucose
  • phillyrin
Topics
  • AMP-Activated Protein Kinase Kinases
  • AMP-Activated Protein Kinases (genetics, metabolism)
  • Glucose (metabolism)
  • Glucosides (pharmacology)
  • Hep G2 Cells
  • Hepatocytes (drug effects, enzymology, metabolism)
  • Humans
  • Lipid Metabolism (drug effects)
  • Plant Extracts (pharmacology)
  • Protein Serine-Threonine Kinases (genetics, metabolism)
  • Signal Transduction (drug effects)

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