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AMPK activation with glabridin ameliorates adiposity and lipid dysregulation in obesity

Title
AMPK activation with glabridin ameliorates adiposity and lipid dysregulation in obesity
Authors
Lee J.-W.Choe S.S.Jang H.Kim J.Jeong H.W.Jo H.Jeong K.-H.Tadi S.Park M.G.Kwak T.H.Kim J.M.Hyun D.-H.Kim J.B.
Ewha Authors
현동훈
SCOPUS Author ID
현동훈scopus
Issue Date
2012
Journal Title
Journal of Lipid Research
ISSN
0022-2275JCR Link
Citation
vol. 53, no. 7, pp. 1277 - 1286
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
In this study, we demonstrate that activation of AMP-activated protein kinase (AMPK) with glabridin alleviates adiposity and hyperlipidemia in obesity. In several obese rodent models, glabridin decreased body weight and adiposity with a concomitant reduction in fat cell size. Further, glabridin ameliorated fatty liver and plasma levels of triglyceride and cholesterol. In accordance with these findings, glabridin suppressed the expression of lipogenic genes such as sterol regulatory element binding transcription factor (SREBP)-1c, fatty acid synthase (FAS), acetyl-CoA carboxylase (ACC), and stearoyl-CoA desaturase (SCD)-1 in white adipose tissues and liver, whereas it elevated the expression of fatty acid oxidation genes such as carnitine palmitoyl transferase (CPT)1, acyl-CoA oxidase (ACO), and peroxisome proliferator-activated receptor (PPAR)α in muscle. Moreover, glabridin enhanced phosphorylation of AMPK in muscle and liver and promoted fatty acid oxidation by modulating mitochondrial activity. Together, these data suggest that glabridin is a novel AMPK activator that would exert therapeutic effects in obesity-related metabolic disorders. Copyright © 2012 by the American Society for Biochemistry and Molecular Biology, Inc.
DOI
10.1194/jlr.M022897
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자연과학대학 > 생명과학전공 > Journal papers
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