title: The inhibition of oleic acid induced hepatic lipogenesis and the promotion of lipolysis by caffeic acid via up-regulation of AMP-activated kinase.
abstract: BACKGROUND
  Caffeic acid (CA) can inhibit toxin-induced liver injury. In this study, CA is assessed for its lipid lowering potential when oleic acid is used to induce non-alcoholic fatty liver disease in human HepG2 cells.
  
  
  RESULTS
  The results showed that both the triglyceride and cholesterol content are decreased in the HepG2 cells by using the enzymatic colorimetric method. CA enhances the phosphorylation of AMP-activated protein kinase (AMPK) and its primary downstream targeting enzyme, acetyl-CoA carboxylase. CA down-regulates the lipogenesis gene expression of sterol regulatory element-binding protein-1 and its target genes, fatty acid synthase in the presence of oleic acid. In addition, CA significantly decreases cholesterol and triglyceride production via inhibition the expression of both 3-hydroxy-3-methyglutary coenzyme A reductase and glycerol-3-phosphate acyltransferase. These effects are eliminated by pretreatment with compound C, an AMPK inhibitor.
  
  
  CONCLUSIONS
  These results demonstrate that CA inhibits oleic acid induced hepatic lipogenesis and the promotion of lipolysis via up-regulation of AMP-activated kinase.
authors.affiliation: Division of Endocrinology and Metabolism, Department of Internal Medicine, Cheng-Ching Hospital, Taichung, Taiwan; Institute of Biochemistry and Biotechnology, College of Medicine, Chung Shan Medical University, Taichung, Taiwan.
authors.forename: Chung-Chia
authors.initials: CC
authors.lastname: Liao
authors.forename: Ting-Tsz
authors.initials: TT
authors.lastname: Ou
authors.forename: Hui-Pei
authors.initials: HP
authors.lastname: Huang
authors.forename: Chau-Jong
authors.initials: CJ
authors.lastname: Wang
mesh_terms: D055372:AMP-Activated Protein Kinases / Q000235:genetics / Q000378:metabolism*; D000103:Acetyl-CoA Carboxylase / Q000378:metabolism; D002109:Caffeic Acids / Q000494:pharmacology* / Q000627:therapeutic use; D002784:Cholesterol / Q000378:metabolism; D004032:Diet; D004041:Dietary Fats / Q000378:metabolism; D054872:Fatty Acid Synthesis Inhibitors / Q000494:pharmacology / Q000627:therapeutic use; D005234:Fatty Liver / Q000378:metabolism* / Q000517:prevention & control; D015870:Gene Expression; D056945:Hep G2 Cells; D006801:Humans; D000960:Hypolipidemic Agents / Q000494:pharmacology / Q000627:therapeutic use; D050155:Lipogenesis / Q000187:drug effects* / Q000235:genetics; D008066:Lipolysis / Q000187:drug effects*; D008099:Liver / Q000187:drug effects / Q000378:metabolism; D065626:Non-alcoholic Fatty Liver Disease; D019301:Oleic Acid / Q000378:metabolism*; D010766:Phosphorylation; D010936:Plant Extracts / Q000494:pharmacology* / Q000627:therapeutic use; D051780:Sterol Regulatory Element Binding Protein 1 / Q000235:genetics / Q000378:metabolism; D014280:Triglycerides / Q000378:metabolism; D015854:Up-Regulation
chemical_list: D002109:Caffeic Acids; D004041:Dietary Fats; D054872:Fatty Acid Synthesis Inhibitors; D000960:Hypolipidemic Agents; D010936:Plant Extracts; D051780:Sterol Regulatory Element Binding Protein 1; D014280:Triglycerides; D019301:Oleic Acid; D002784:Cholesterol; D055372:AMP-Activated Protein Kinases; D000103:Acetyl-CoA Carboxylase; C040048:caffeic acid
keywords: AMP-activated protein kinase (AMPK); caffeic acid (CA); hepatic lipogenesis; hepatic lipolysis; non-alcoholic fatty liver disease (NAFLD)