These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Compound K, a novel ginsenoside metabolite, inhibits adipocyte differentiation in 3T3-L1 cells: involvement of angiogenesis and MMPs.
    Author: Park D, Yoon M.
    Journal: Biochem Biophys Res Commun; 2012 Jun 01; 422(2):263-7. PubMed ID: 22575448.
    Abstract:
    Compound K, a novel ginsenoside metabolite formed by intestinal bacteria, is shown to inhibit angiogenesis and matrix metalloproteinase (MMP) activities. Since growth and development of adipose tissue are thought to require adipogenesis, angiogenesis, and extracellular matrix remodeling, we investigated whether compound K inhibits adipocyte differentiation and its potential mechanisms. Treatment of 3T3-L1 adipocytes with compound K inhibited lipid accumulation and expression of adipocyte-specific genes (i.e., PPARγ, leptin, aP2, and C/EBPα). Compound K decreased mRNA levels of angiogenic factors (i.e., VEGF-A and FGF-2) and MMPs (i.e., MMP-2 and MMP-9), whereas it increased mRNA levels of angiogenic inhibitors (TSP-1, TIMP-1, and TIMP-2) in 3T3-L1 cells. MMP-2 and MMP-9 activities were also decreased in compound K-treated cells. These results demonstrate that compound K effectively inhibited adipogenesis and that this process may be mediated in part through changes in the expression of genes involved in angiogenesis and MMP system. Thus, by suppressing adipogenesis, compound K likely has therapeutic potential for the treatment of obesity and related disorders.
    [Abstract] [Full Text] [Related] [New Search]