These authors contributed equally to this work.
3-Caffeoyl, 4-dihydrocaffeoylquinic acid from Salicornia herbacea attenuates high glucose-induced hepatic lipogenesis in human HepG2 cells through activation of the liver kinase B1 and silent information regulator T1/AMPK-dependent pathway
Article first published online: 24 JAN 2013
© 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
Molecular Nutrition & Food Research
Volume 57, Issue 3, pages 471–482, March 2013
How to Cite
Pil Hwang, Y., Gyun Kim, H., Choi, J. H., Truong Do, M., Tran, T. P., Chun, H. K., Chung, Y. C., Jeong, T. C. and Jeong, H. G. (2013), 3-Caffeoyl, 4-dihydrocaffeoylquinic acid from Salicornia herbacea attenuates high glucose-induced hepatic lipogenesis in human HepG2 cells through activation of the liver kinase B1 and silent information regulator T1/AMPK-dependent pathway. Mol. Nutr. Food Res., 57: 471–482. doi: 10.1002/mnfr.201200529
- Issue published online: 12 MAR 2013
- Article first published online: 24 JAN 2013
- Manuscript Revised: 9 NOV 2012
- Manuscript Accepted: 9 NOV 2012
- Manuscript Received: 7 AUG 2012
- Korean Health Technology R&D Project. Grant Number: A111580
- Ministry of Health & Welfare
- National Research Foundation of Korea. Grant Number: 2010–00266220
Vol. 57, Issue 5, 928, Article first published online: 16 APR 2013
- 3-Caffeoyl, 4-dihydrocaffeoylquinic acid;
- High glucose;
Increasing evidence indicates that polyphenols may protect against metabolic disease through activating AMP-activated protein kinase (AMPK). The aims of our study were to provide new data on the molecular mechanism(s) underlying the role of the phenolic compound, 3-caffeoyl, 4-dihydrocaffeoylquinic acid (CDCQ) from Salicornia herbacea, in the prevention of high glucose-induced lipogenesis in human HepG2 cells.
Methods and results
Nile red staining assays were used to demonstrate lipid accumulation in the cells. Expression of sterol regulatory element-binding protein-1c (SREBP-1c) and fatty acid synthase (FAS) gene at the levels of promoter activity, mRNA, and protein was demonstrated using transient transfection assays, quantitative RT-PCR, and Western blot analyses, respectively. We found that CDCQ suppressed high glucose-induced lipid accumulation in HepG2 cells. CDCQ strongly inhibited high glucose-induced FAS expression by modulating SREBP-1c activation. Moreover, the use of both a specific inhibitor and liver kinase B1 (LKB1)-siRNA transfected HepG2 cells showed that CDCQ activated AMPK via silent information regulator T1 (SIRT1) or LKB1 in HepG2 cells.
These results indicate that CDCQ prevented lipid accumulation by blocking the expression of SREBP-1c and FAS through LKB1/SIRT1 and AMPK activation in HepG2 cells, suggesting that CDCQ plays a potential role in the prevention of lipogenesis by AMPK activation.