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

Title
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
Author(s)
정태천황용필[황용필]김형균[김형균]최재호[최재호]Minh T. Do[Minh T. Do]Thu P. Tran[Thu P. Tran]천효곤[천효곤]정영철[정영철]정혜광[정혜광]
Keywords
PROTEIN-KINASE; LIPID-METABOLISM; ADIPOSE-TISSUE; FATTY LIVER; AMPK; LXR; RECEPTOR; OBESITY; SIRT1; LKB1
Issue Date
201303
Publisher
WILEY-BLACKWELL
Citation
MOLECULAR NUTRITION & FOOD RESEARCH, v.57, no.3, pp.471 - 482
Abstract
Scope 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. Conclusion 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.
URI
http://hdl.handle.net/YU.REPOSITORY/26216http://dx.doi.org/10.1002/mnfr.201200529
ISSN
1613-4125
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약학대학 > 약학부 > Articles
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