Licochalcone A regulates hepatic lipid metabolism through activation of AMP-activated protein kinase
| Autor: | Sung Hyun Chung, Hai Yan Quan, Go Woon Kim, Hee Kyung Jo, Do Yeon Kim, Soo Jung Kim |
|---|---|
| Rok vydání: | 2013 |
| Předmět: |
medicine.medical_specialty
Licochalcone A CD36 Gene Expression AMP-Activated Protein Kinases Diet High-Fat Mice chemistry.chemical_compound Adenosine Triphosphate Chalcones Oxygen Consumption AMP-activated protein kinase Internal medicine Drug Discovery Glycyrrhiza medicine Animals Humans Protein kinase A Triglycerides Pharmacology chemistry.chemical_classification Mice Inbred ICR biology Plant Extracts Fatty acid AMPK Biological Transport Hep G2 Cells General Medicine Lipid Metabolism Dietary Fats Mitochondria Enzyme Activation Fatty acid synthase Endocrinology Liver chemistry Lipogenesis biology.protein Sterol Regulatory Element Binding Protein 1 Signal Transduction |
| Zdroj: | Fitoterapia. 86:208-216 |
| ISSN: | 0367-326X |
| Popis: | Licochalcone A (LA) is a major phenolic ingredient of Glycyrrhiza plant. Although multiple pharmacological activities of LA have been reported, effect on hepatic lipid metabolism is unknown yet. The present study showed LA to suppress the hepatic triglyceride accumulation in HepG2 cells and ICR mice fed on a high fat diet (HFD). LA inhibited lipogenesis via suppression of sterol regulatory element-binding protein 1c (SREBP1c) and its target enzymes (stearoyl-CoA desaturase 1, fatty acid synthase and glycerol-3-phosphate acyltransferase) transcription. In addition, LA up-regulated gene expression of proteins such as peroxisome proliferator-activated receptor α (PPARα) and fatty acid transporter (FAT/CD36), which are responsible for lipolysis and fatty acid transport, respectively. These effects were mediated through activation of AMP-activated protein kinase (AMPK), and were abrogated when HepG2 cells were treated with an AMPK inhibitor, compound C. To explore how LA activates AMPK, oxygen consumption rate and ATP levels were measured in HepG2 cells. LA significantly inhibited the mitochondrial respiration and ATP levels, suggesting that LA activated AMPK indirectly. In animal study, LA (5 and 10 mg/kg) was orally administered to six-week-old mice once a day for 3 weeks. In vitro results were likely to hold true in vivo experiment, as LA markedly lowered the triglyceride levels and activated AMPK signaling pathway in the liver of ICR mice fed on a HFD. In conclusion, the current study suggests that LA suppressed hepatic triglyceride accumulation through modulation of AMPK-SREBP signaling pathway and thus LA may be a potential therapeutic agent for treating fatty liver disease. |
| Databáze: | OpenAIRE |
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