Mulberry anthocyanins inhibit oleic acid induced lipid accumulation by reduction of lipogenesis and promotion of hepatic lipid clearance

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[1] Chang, Jia-Jen
[2] Hsu, Man-Jung
[3] Huang, Hui-Pei
[4] Chung, Dai-Jung
[5] 1,Chang, Yun-Ching
[6] 1,Wang, Chau-Jong
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Chang, Y.-C. (changyc@csmu.edu.tw) | 1600年 / American Chemical Society卷 / 61期
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Mulberry (Morus alba L.) has been considered to possess different benefits such as protecting liver; improving fever; urine excretion disorder; hypertension; and diabetic syndrome; and preventing cardiovascular diseases. Recently; mounting evidence has shown that mulberry anthocyanin extract (MAE) is beneficial to hyperlipidemia; however; the mechanisms remain unclear. The present study was aimed to investigate the protective effects of MAE on hepatocyte cultured with high fatty acid and the underlying mechanisms. By using human hepatoma cell HepG2 as cell model; the results showed that MAE suppressed fatty acid synthesis and enhanced fatty acid oxidation; contributing to amelioration of lipid accumulation induced by oleic acid (OA). Moreover; MAE also inhibited acetyl coenzyme A carboxylase (ACC) activities by stimulating adenosine monophosphate-activated protein kinase (AMPK). MAE attenuated the expression of sterol regulatory element-binding protein-1 (SREBP-1) and its target molecules; such as fatty acid synthase (FAS). Similar results were also found in the expressions of enzymes involved in triglyceride and cholesterol biosyntheses including glycerol-3-phosphate acyltransferase (GPAT); 3-hydroxy-3-methyl-glutaryl CoA reductase (HMGCoR); adipocyte-specific fatty acid binding protein (A-FABP); and SREBP-2. In contrast; the lipolytic enzyme expressions of peroxisome proliferator activated receptor α (PPARα) and carnitinepalmitol- transferase-1 (CPT1) were increased. This study suggests the hypolipidemic effects of MAE occur via phosphorylation of AMPK and inhibition of lipid biosynthesis and stimulation of lipolysis. Therefore; the mulberry anthocyanins may actively prevent nonalcoholic fatty liver disease. © 2013 American Chemical Society;
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