AMPK activation with glabridin ameliorates adiposity and lipid dysregulation in obesity

Joo Won Lee, Sung Sik Choe, Hagoon Jang, Jiyeong Kim, Hyun Woo Jeong, Hyunsun Jo, Kyeong Hoon Jeong, Surendar Tadi, Myoung Gyu Park, Tae Hwan Kwak, Jin Man Kim, Dong Hoon Hyun, Jae Bum Kim

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82 Scopus citations


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.

Original languageEnglish
Pages (from-to)1277-1286
Number of pages10
JournalJournal of Lipid Research
Issue number7
StatePublished - Jul 2012


  • AMP-activated protein kinase
  • Fatty acid oxidation
  • Fatty liver


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