inhibition of oleic acid induced hepatic lipogenesis and the promotion of lipolysis by caffeic acid via up‐regulation of AMP‐activated kinase

• Published in: Journal of the science of food and agriculture Vol. 94; no. 6; pp. 1154 - 1162
• Main Authors: Liao, Chung‐Chia, Ou, Ting‐Tsz, Huang, Hui‐Pei, Wang, Chau‐Jong
• Format: Journal Article
• Language: English
• Published: Chichester, UK John Wiley & Sons, Ltd 01-04-2014; John Wiley and Sons, Limited
• Subjects: Acetyl-CoA Carboxylase - metabolism; AMP-activated protein kinase (AMPK); AMP-Activated Protein Kinases - genetics; AMP-Activated Protein Kinases - metabolism; caffeic acid; caffeic acid (CA); Caffeic Acids - pharmacology; Caffeic Acids - therapeutic use; Cells; Cholesterol; Cholesterol - metabolism; colorimetry; Diet; Dietary Fats - metabolism; Fatty Acid Synthesis Inhibitors - pharmacology; Fatty Acid Synthesis Inhibitors - therapeutic use; fatty liver; Fatty Liver - metabolism; Fatty Liver - prevention & control; fatty-acid synthase; Gene Expression; gene expression regulation; genes; Hep G2 Cells; hepatic lipogenesis; hepatic lipolysis; Humans; Hypolipidemic Agents - pharmacology; Hypolipidemic Agents - therapeutic use; Inhibition; Inhibitors; Kinases; lipogenesis; Lipogenesis - drug effects; Lipogenesis - genetics; lipolysis; Lipolysis - drug effects; Liver; Liver - drug effects; Liver - metabolism; Liver diseases; Non-alcoholic Fatty Liver Disease; non-alcoholic fatty liver disease (NAFLD); Oleic acid; Oleic Acid - metabolism; Phosphorylation; Plant Extracts - pharmacology; Plant Extracts - therapeutic use; Promotion; protein kinases; Sterol Regulatory Element Binding Protein 1 - genetics; Sterol Regulatory Element Binding Protein 1 - metabolism; Toxins; Triglycerides; Triglycerides - metabolism; Up-Regulation; non-alcoholic fatty liver disease (NAFLD); hepatic lipogenesis; AMP-activated protein kinase (AMPK); caffeic acid (CA); hepatic lipolysis
• ISSN: 0022-5142; 1097-0010
• DOI: 10.1002/jsfa.6386

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. © 2013 Society of Chemical Industry