Ethyl Acetate Fraction of Amomum xanthioides Ameliorates Nonalcoholic Fatty Liver Disease in a High-Fat Diet Mouse Model

Nutrients. 2020 Aug 13;12(8):2433. doi: 10.3390/nu12082433.

Abstract

The global prevalence of nonalcoholic fatty liver disease (NAFLD) is estimated to be 25% and has continued to increase; however, no drugs have yet been approved for NAFLD treatments. The ethyl acetate fraction of Amomum xanthioides (EFAX) was previously reported to have an anti-hepatic fibrosis effect, but its effects on steatosis or steatohepatitis remain unclear. This study investigated the anti-fatty liver of EFAX using a high-fat diet mouse model. High-fat diet intake for 8 weeks induced hepatic steatosis with mild inflammation and oxidative damage and increased the adipose tissue weight along with the development of dyslipidemia. EFAX treatment significantly ameliorated the steatohepatic changes, the increased weight of adipose tissues, and the altered serum lipid profiles. These observed effects were possibly due to the lipolysis-dominant activity of EFAX on multiple hepatic proteins including sterol regulatory element-binding protein (mSREBP)-1c, peroxisome proliferator-activated receptor (PPAR)-α, AMP-activated protein kinase, and diglyceride acyltransferases (DGATs). Taken together, these results show that EFAX might be a potential therapeutic agent for regulating a wide spectrum of NAFLDs from steatosis to fibrosis via multiple actions on lipid metabolism-related proteins. Further studies investigating clear mechanisms and their active compounds are needed.

Keywords: Amomum xanthioides; NAFLD; NASH; fatty liver; herb.

MeSH terms

  • AMP-Activated Protein Kinases / metabolism
  • Acetates / pharmacology*
  • Amomum / chemistry*
  • Animals
  • Diacylglycerol O-Acyltransferase / metabolism
  • Diet, High-Fat / adverse effects
  • Disease Models, Animal
  • Lipid Metabolism / drug effects*
  • Lipids / blood
  • Lipolysis / drug effects
  • Liver / metabolism
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Non-alcoholic Fatty Liver Disease / drug therapy*
  • Non-alcoholic Fatty Liver Disease / etiology
  • PPAR alpha / metabolism
  • Sterol Regulatory Element Binding Protein 1 / metabolism

Substances

  • Acetates
  • Lipids
  • PPAR alpha
  • Srebf1 protein, mouse
  • Sterol Regulatory Element Binding Protein 1
  • ethyl acetate
  • Diacylglycerol O-Acyltransferase
  • AMP-Activated Protein Kinases