1. Academic Validation
  2. Chrysophanic Acid Suppresses Adipogenesis and Induces Thermogenesis by Activating AMP-Activated Protein Kinase Alpha In vivo and In vitro

Chrysophanic Acid Suppresses Adipogenesis and Induces Thermogenesis by Activating AMP-Activated Protein Kinase Alpha In vivo and In vitro

  • Front Pharmacol. 2016 Dec 8;7:476. doi: 10.3389/fphar.2016.00476.
Hara Lim 1 Jinbong Park 1 Hye-Lin Kim 1 JongWook Kang 1 Mi-Young Jeong 1 Dong-Hyun Youn 1 Yunu Jung 1 Yong-Il Kim 2 Hyun-Ju Kim 1 Kwang Seok Ahn 1 Su-Jin Kim 3 Seong-Kyu Choe 2 Seung-Heon Hong 4 Jae-Young Um 1
Affiliations

Affiliations

  • 1 College of Korean Medicine, Basic Research Laboratory for Comorbidity Regulation Kyung Hee University, Seoul, South Korea.
  • 2 Department of Microbiology and Center for Metabolic Function Regulation, School of Medicine, Wonkwang University Iksan, South Korea.
  • 3 Department of Cosmeceutical Science, Daegu Haany University Kyungsan, South Korea.
  • 4 Department of Pharmacology, College of Pharmacy, Wonkwang University Iksan, South Korea.
Abstract

Chrysophanic acid (CA) is a member of the anthraquinone family abundant in rhubarb, a widely used herb for obesity treatment in Traditional Korean Medicine. Though several studies have indicated numerous features of CA, no study has yet reported the effect of CA on obesity. In this study, we tried to identify the anti-obesity effects of CA. By using 3T3-L1 adipocytes and primary cultured brown adipocytes as in vitro models, high-fat diet (HFD)-induced obese mice, and zebrafish as in vivo models, we determined the anti-obesity effects of CA. CA reduced weight gain in HFD-induced obese mice. They also decreased lipid accumulation and the expressions of adipogenesis factors including Peroxisome Proliferator-activated Receptor gamma (PPARγ) and CCAAT/enhancer-binding protein alpha (C/EBPα) in 3T3-L1 adipocytes. In addition, uncoupling protein 1 (UCP1) and Peroxisome Proliferator-activated Receptor gamma coactivator 1-alpha (PGC1α), the brown fat specific thermogenic genes, were up-regulated in brown adipocytes by CA treatment. Furthermore, when co-treated with Compound C, the AMP-activated protein kinase (AMPK) inhibitor, the action of CA on AMPKα was nullified in both types of adipocytes, indicating the multi-controlling effect of CA was partially via the AMPKα pathway. Given all together, these results indicate that CA can ameliorate obesity by controlling the adipogenic and thermogenic pathway at the same time. On these bases, we suggest the new potential of CA as an anti-obese pharmacotherapy.

Keywords

AMP-activated protein kinase alpha; adipogenesis; chrysophanic acid; obesity; thermogenesis.

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