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Cited by 343

The DOI matches its Crossref record; 6 of the 6 references it cites were found in a registry or an index.

Inhibition of lipid synthesis through activation of AMP kinase: an additional mechanism for the hypolipidemic effects of berberine

Open access
Brusq, Jean-Marie, Ancellin, Nicolas, Grondin, Pascal, Guillard, Raphaelle, Martin, Sandrine, Saintillan, Yannick, Issandou, Marc·2006·Journal of Lipid Research

Abstract

The alkaloid drug berberine (BBR) was recently described to decrease plasma cholesterol and triglycerides (TGs) in hypercholesterolemic patients by increasing expression of the hepatic low density lipoprotein receptor (LDLR). Using HepG2 human hepatoma cells, we found that BBR inhibits cholesterol and TG synthesis in a similar manner to the AMP-activated protein kinase (AMPK) activator 5-aminoimidazole-4-carboxamide 1-beta-ribofuranoside (AICAR). Significant increases in AMPK phosphorylation and AMPK activity were observed when the cells were incubated with BBR. Activation of AMPK was also demonstrated by measuring the phosphorylation of acetyl-CoA carboxylase, a substrate of AMPK, correlated with a subsequent increase in fatty acid oxidation. All of these effects were abolished by the mitogen-activated protein kinase kinase inhibitor PD98059. Treatment of hyperlipidemic hamsters with BBR decreased plasma LDL cholesterol and strongly reduced fat storage in the liver. These findings indicate that BBR, in addition to upregulating the LDLR, inhibits lipid synthesis in human hepatocytes through the activation of AMPK. These effects could account for the strong reduction of plasma TGs observed with this drug in clinical trials.

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Crossref · 10.1194/jlr.m600020-jlr200

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Metadata

Authors
Brusq, J.-M., Ancellin, N., Grondin, P., Guillard, R., Martin, S., Saintillan, Y., & Issandou, M.
Venue
Journal of Lipid Research
Publisher
Elsevier BV
Published
2006-06
Volume
47
Issue
6
Pages
1281-1288
ISSN
0022-2275 (ISSN-L)
OpenAlex
W1984985876
Cited by
343
References
6
FWCI
9.06
Type
journal article
Language
en
Open access
hybrid

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