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Evidence-Based Complementary and Alternative Medicine
Volume 2018 (2018), Article ID 7420265, 8 pages
Research Article

Nobiletin Inhibits Hepatic Lipogenesis via Activation of AMP-Activated Protein Kinase

1Division of Food and Animal Sciences, Chungbuk National University, Cheongju, Chungbuk 28644, Republic of Korea
2School of Food Biotechnology and Nutrition, Kyungsung University, Busan 48434, Republic of Korea

Correspondence should be addressed to Junsoo Lee

Received 29 September 2017; Revised 22 December 2017; Accepted 11 January 2018; Published 7 February 2018

Academic Editor: Luciana Dini

Copyright © 2018 Taewon Yuk et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


We aimed to investigate the effects of nobiletin on hepatic lipogenesis in high glucose-induced lipid accumulation in HepG2 cells. Nobiletin, a citrus polymethoxyflavonoid with six methoxy groups, is present abundantly in the peels of citrus fruits. HepG2 cells were incubated in Dulbecco’s modified Eagle’s medium containing high glucose (25 mM) and subsequently treated with nobiletin at different concentrations (5, 25, and 50 μM). Results showed that nobiletin markedly inhibited high glucose-induced hepatic lipid accumulation in HepG2 cells. In addition, it reduced the protein expression of lipogenic factors, including sterol regulatory element-binding protein 1c (SREBP-1c) and fatty acid synthase (FAS). Nobiletin significantly increased the phosphorylation of AMP-activated protein kinase (AMPK) and acetyl-CoA carboxylase. Pretreatment with compound C, an AMPK inhibitor, abolished the inhibitory effects of nobiletin on SREBP-1c and FAS expression. These results suggested that nobiletin might attenuate high glucose-induced lipid accumulation in HepG2 hepatocytes via modulation of AMPK signaling pathway. Therefore, nobiletin might be useful for the prevention and treatment of nonalcoholic fatty liver diseases.