z-logo
Premium
Decursin, an Active Compound Isolated from Angelica gigas , Inhibits Fat Accumulation, Reduces Adipocytokine Secretion and Improves Glucose Tolerance in Mice Fed a High‐Fat Diet
Author(s) -
Hwang JinTaek,
Kim Sung Hee,
Hur Haeng Jeon,
Kim Hyun Jin,
Park Jae Ho,
Sung Mi Jeong,
Yang Hye Jeong,
Ryu Shi Yong,
Kim Young Sup,
Cha Mi Ran,
Kim Myung Sunny,
Kwon Dae Young
Publication year - 2012
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.3612
Subject(s) - resistin , endocrinology , medicine , triglyceride , adipocyte , leptin , adipokine , glucose tolerance test , cholesterol , diabetes mellitus , pharmacology , adipose tissue , obesity , insulin resistance
Decursin (De), an active component of Angelica gigas , is known to exert anticancer and neuroprotective effects. However, its antiobesity and antidiabetic potential has not yet been investigated. This study evaluated the antiobesity effect of decursin, particularly focusing on its ability to inhibit adipocyte differentiation in 3 T3‐L1 cells. Decursin treatment resulted in the inhibition of adipocyte differentiation and the expression of fatty acid synthase. The study further investigated these antiobesity effects using mice fed a normal diet (ND), a high‐fat diet (HFD) and a HFD plus decursin 200 mg/kg diet (HFD + De) for 7 weeks. Mice administered HFD plus decursin showed a drastic decrease in weight gain, triglyceride content, total cholesterol content and fat size compared with those that received the HFD alone; this was observed despite similar quantities of total food intake. Furthermore, decursin improved glucose tolerance in mice fed a HFD. Finally, administration of decursin along with the HFD significantly reduced the secretion of HFD‐induced adipocytokines such as leptin, resistin, IL‐6 and MCP‐1. These results suggest that decursin might be useful for the treatment of obesity and diabetes. Copyright © 2011 John Wiley & Sons, Ltd.

This content is not available in your region!

Continue researching here.

Having issues? You can contact us here