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.
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Authors | Minh Truong Do, Hyung Gyun Kim, Jae Ho Choi, Tilak Khanal, Bong Hwan Park, Thu Phuong Tran, Yong Pil Hwang, Minkyun Na, Hye Gwang Jeong |
Journal | Food chemistry
(Food Chem)
Vol. 136
Issue 2
Pg. 415-25
(Jan 15 2013)
ISSN: 1873-7072 [Electronic] England |
PMID | 23122079
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Copyright | Copyright © 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
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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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