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Purple sweet potato anthocyanins attenuate hepatic lipid accumulation through activating adenosine monophosphate–activated protein kinase in human HepG2 cells and obese mice
Authors:Yong Pil Hwang  Jae Ho Choi  Eun Hee Han  Hyung Gyun Kim  Ji-Hyang Wee  Kyung Ok Jung  Kyung Hee Jung  Kwang-il Kwon  Tae Cheon Jeong  Young Chul Chung  Hye Gwang Jeong
Institution:aDepartment of Toxicology, College of Pharmacy, Chungnam National University, Daejeon 305-764, Republic of Korea;bJeonnam Bioindustry Foundation, Biofood Technology Center, Naju-city, Jeollanamdo, Republic of Korea;cCollege of Pharmacy, Yeungnam University, Kyungsan, Republic of Korea;dDepartment of Pharmaceutical Engineering, International University of Korea, Jinju, Republic of Korea;eDepartment of Food Science, International University of Korea, Jinju, Republic of Korea
Abstract:Purple sweet potato is a functional food rich in anthocyanins that possess disease-preventive properties. Anthocyanins are known to possess potent antidiabetic properties. However, the effect of the anthocyanin fraction (AF) from purple sweet potato on hepatic lipid metabolism remains unclear. Our hypothesis is that AF inhibits hepatic lipid accumulation through the activation of adenosine monophosphate–activated protein kinase (AMPK) signaling pathways in vitro and in vivo. In this study, we evaluated body weight, liver histology, and hepatic lipid content in high-fat diet (HFD)–fed ICR mice treated with AF. In addition, we characterized the underlying mechanism of AF's effects in HepG2 hepatocytes through Western blot analysis. Anthocyanin fraction (200 mg/kg per day) reduced weight gain and hepatic triglyceride accumulation and improved serum lipid parameters in mice fed an HFD for 4 weeks. Anthocyanin fraction significantly increased the phosphorylation of AMPK and acetyl-coenzyme A carboxylase (ACC) in the liver and HepG2 hepatocytes. In addition, AF down-regulated the levels of sterol regulatory element-binding protein 1 and its target genes including ACC and fatty acid synthase (FAS). The specific AMPK inhibitor compound C attenuated the effects of AF on the expression of lipid metabolism–related proteins such as SREBP-1 and FAS in HepG2 hepatocytes. The beneficial effects of AF on HFD-induced hepatic lipid accumulation are thus mediated through AMPK signaling pathways, suggesting a potential target for the prevention of obesity.
Keywords:Abbreviations: ACC  acetyl-coenzyme A carboxylase  AF  anthocyanin fraction  ALT  alanine aminotransferase  AMPK  adenosine monophosphate&ndash  activated protein kinase  AST  aspartate aminotransferase  CoA  coenzyme A  C3G  cyanidin-3-glucoside  DMEM  Dulbecco modified Eagle medium  FAS  fatty acid synthase  HFD  high-fat diet  LDH  lactate dehydrogenase  ND  normal diet  PSP  purple sweet potato  SREBP  sterol regulatory element-binding protein  TBARS  thiobarbituric acid reactive substance
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