4.6 Article

Arctigenin Inhibits Adipogenesis by Inducing AMPK Activation and Reduces Weight Gain in High-Fat Diet-Induced Obese Mice

Journal

JOURNAL OF CELLULAR BIOCHEMISTRY
Volume 117, Issue 9, Pages 2067-2077

Publisher

WILEY
DOI: 10.1002/jcb.25509

Keywords

ARCTIGENIN; 3T3-L1; hAMSCs; HFD-INDUCED OBESE MICE; AMPK

Funding

  1. National Research Foundation of Korea (NRF) [2011-0030130, 2013R1A2A2A01067805, NRF-2015R1A4A1042399]
  2. National Research Foundation of Korea [2013R1A2A2A01067805] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Although arctigenin (ARC) has been reported to have some pharmacological effects such as anti-inflammation, anti-cancer, and antioxidant, there have been no reports on the anti-obesity effect of ARC. The aim of this study is to investigate whether ARC has an anti-obesity effect and mediates the AMP-activated protein kinase (AMPK) pathway. We investigated the anti-adipogenic effect of ARC using 3T3-L1 pre-adipocytes and human adipose tissue-derived mesenchymal stem cells (hAMSCs). In high-fat diet (HFD)-induced obese mice, whether ARC can inhibit weight gain was investigated. We found that ARC reduced weight gain, fat pad weight, and triglycerides in HFD-induced obese mice. ARC also inhibited the expression of peroxisome proliferator-activated receptor gamma (PPAR) and CCAAT/enhancer-binding protein alpha (C/EBP) in in vitro and in vivo. Furthermore, ARC induced the AMPK activation resulting in down-modulation of adipogenesis-related factors including PPAR, C/EBP, fatty acid synthase, adipocyte fatty acid-binding protein, and lipoprotein lipase. This study demonstrates that ARC can reduce key adipogenic factors by activating the AMPK in vitro and in vivo and suggests a therapeutic implication of ARC for obesity treatment. J. Cell. Biochem. 117: 2067-2077, 2016. (c) 2016 Wiley Periodicals, Inc.

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