Purple sweet potato anthocyanins attenuate hepatic lipid accumulation through activating adenosine monophosphate–activated protein kinase in human HepG2 cells and obese mice |
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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 |
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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 |
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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. |
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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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