title: Mulberry extract inhibits oleic acid-induced lipid accumulation via reduction of lipogenesis and promotion of hepatic lipid clearance.
abstract: BACKGROUND
  Mulberries are a traditional edible food used to treat hepatic disease. The anti-obesity and hypolipidemic effects of mulberry water extracts (MWE) have attracted increasing interest. In the present study, MWE were assessed for their hepatic lipid-lowering potential when administered in fatty acid overload conditions in HepG2 cells.
  
  
  RESULTS
  We found that MWE significantly reduced lipid accumulation, suppressed fatty acid synthesis, and stimulated fatty acid oxidation. Furthermore, MWE also inhibited acetyl coenzyme A carboxylase activities by stimulating adenosine monophosphate-activated protein kinase (AMPK). MWE attenuated the expression of sterol regulatory element-binding protein-1 (SREBP-1) and its target molecules, such as fatty acid synthase. Similar results were also measured in the expressions of enzymes involved in triglyceride and cholesterol biosyntheses including glycerol-3-phosphate acyltransferase, 3-hydroxy-3-methylglutaryl-CoA reductase, and SREBP-2. In contrast, the lipolytic enzyme expression of peroxisome proliferator activated receptor α and carnitine palmitoyltransferase-1 were increased.
  
  
  CONCLUSIONS
  Our study suggests that the hypolipidemic effects of MWE occur via phosphorylation of AMPK and inhibition of lipid biosynthesis. Therefore, the mulberry extract may be active in the prevention of fatty liver.
authors: Institute of Biochemistry and Biotechnology, College of Medicine, Chung Shan Medical University, Taichung, Taiwan.
authors: Ting-Tsz
authors: TT
authors: Ou
authors: Man-Jung
authors: MJ
authors: Hsu
authors: Kuei-Chuan
authors: KC
authors: Chan
authors: Chien-Ning
authors: CN
authors: Huang
authors: Hsieh-Hsun
authors: HH
authors: Ho
authors: Chau-Jong
authors: CJ
authors: Wang
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000378:metabolism; D000103:Acetyl-CoA Carboxylase / Q000378:metabolism; D002334:Carnitine O-Palmitoyltransferase / Q000378:metabolism; D002784:Cholesterol / Q000096:biosynthesis; D004041:Dietary Fats / Q000378:metabolism; D004789:Enzyme Activation / Q000187:drug effects; D004791:Enzyme Inhibitors / Q000494:pharmacology; D064429:Fatty Acid Synthases / Q000378:metabolism; D005638:Fruit; D056945:Hep G2 Cells; D006801:Humans; D006949:Hyperlipidemias / Q000188:drug therapy* / Q000378:metabolism; D000960:Hypolipidemic Agents / Q000494:pharmacology / Q000627:therapeutic use; D050356:Lipid Metabolism / Q000187:drug effects*; D015227:Lipid Peroxidation / Q000187:drug effects; D050155:Lipogenesis / Q000187:drug effects*; D008099:Liver / Q000201:enzymology / Q000378:metabolism*; D031625:Morus; D019301:Oleic Acid / Q000378:metabolism / Q000494:pharmacology; D047493:PPAR alpha / Q000378:metabolism; D008517:Phytotherapy; D010936:Plant Extracts / Q000494:pharmacology / Q000627:therapeutic use*; D051780:Sterol Regulatory Element Binding Protein 1 / Q000378:metabolism; D014280:Triglycerides / Q000096:biosynthesis
chemical_list: D004041:Dietary Fats; D004791:Enzyme Inhibitors; D000960:Hypolipidemic Agents; D047493:PPAR alpha; D010936:Plant Extracts; C497387:SREBF1 protein, human; D051780:Sterol Regulatory Element Binding Protein 1; D014280:Triglycerides; D019301:Oleic Acid; D002784:Cholesterol; D002334:Carnitine O-Palmitoyltransferase; D064429:Fatty Acid Synthases; D055372:AMP-Activated Protein Kinases; D000103:Acetyl-CoA Carboxylase