Protective effects of licochalcone a ameliorates obesity and non-alcoholic fatty liver disease via promotion of the sirt-1/AMPK pathway in mice fed a high-fat diet

Chian Jiun Liou, Yau Ker Lee, Nai Chun Ting, Ya Ling Chen, Szu Chuan Shen, Shu Ju Wu*, Wen Chung Huang

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

113 Citations (Scopus)

Abstract

Licochalcone A is a chalcone isolated from Glycyrrhiza uralensis. It showed anti-tumor and anti-inflammatory properties in mice with acute lung injuries and regulated lipid metabolism through the activation of AMP-activated protein kinase (AMPK) in hepatocytes. However, the effects of licochalcone A on reducing weight gain and improving nonalcoholic fatty liver disease (NAFLD) are unclear. Thus, the present study investigated whether licochalcone A ameliorated weight loss and lipid metabolism in the liver of high-fat diet (HFD)-induced obese mice. Male C57BL/6 mice were fed an HFD to induce obesity and NAFLD, and then were injected intraperitoneally with licochalcone A. In another experiment, a fatty liver cell model was established by incubating HepG2 hepatocytes with oleic acid and treating the cells with licochalcone A to evaluate lipid metabolism. Our results demonstrated that HFD-induced obese mice treated with licochalcone A had decreased body weight as well as inguinal and epididymal adipose tissue weights compared with HFD-treated mice. Licochalcone A also ameliorated hepatocyte steatosis and decreased liver tissue weight and lipid droplet accumulation in liver tissue. We also found that licochalcone A significantly regulated serum triglycerides, low-density lipoprotein, and free fatty acids, and decreased the fasting blood glucose value. Furthermore, in vivo and in vitro, licochalcone A significantly decreased expression of the transcription factor of lipogenesis and fatty acid synthase. Licochalcone A activated the sirt-1/AMPK pathway to reduce fatty acid chain synthesis and increased lipolysis and βoxidation in hepatocytes. Licochalcone A can potentially ameliorate obesity and NAFLD in mice via activation of the sirt1/AMPK pathway.

Original languageEnglish
Article number447
JournalCells
Volume8
Issue number5
DOIs
Publication statusPublished - 2019 May

Keywords

  • AMPK
  • HepG2
  • Licochalcone a
  • Lipolysis
  • Nonalcoholic fatty liver disease
  • Obesity

ASJC Scopus subject areas

  • General Medicine

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