AMPK activation with glabridin ameliorates adiposity and lipid dysregulation in obesity

• Main Authors: 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
• Format: Article
• Language: English
• Published: Elsevier 2012-07-01
• Series: Journal of Lipid Research
• Subjects: AMP-activated protein kinase; fatty acid oxidation; fatty liver
• Online Access: http://www.sciencedirect.com/science/article/pii/S0022227520345041

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.