1. 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
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Pil Hwang Y, Gyun Kim H, Choi JH, Truong Do M, Tran TP, Chun HK, Chung YC, Jeong TC, and Jeong HG
- Subjects
- AMP-Activated Protein Kinase Kinases, Chlorogenic Acid pharmacology, Enzyme Activation drug effects, Fatty Acid Synthase, Type I genetics, Fatty Acid Synthase, Type I metabolism, Gene Expression Regulation drug effects, Hep G2 Cells drug effects, Hep G2 Cells metabolism, Humans, Lipid Metabolism drug effects, Promoter Regions, Genetic, RNA, Small Interfering, Signal Transduction drug effects, Sirtuin 1 genetics, Sirtuin 1 metabolism, Sterol Regulatory Element Binding Protein 1 genetics, Sterol Regulatory Element Binding Protein 1 metabolism, AMP-Activated Protein Kinases metabolism, Chenopodiaceae chemistry, Chlorogenic Acid analogs & derivatives, Glucose adverse effects, Lipogenesis drug effects, Protein Serine-Threonine Kinases metabolism
- 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., (© 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)
- Published
- 2013
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