title: Compound K, a novel ginsenoside metabolite, inhibits adipocyte differentiation in 3T3-L1 cells: involvement of angiogenesis and MMPs.
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.
authors.affiliation: Department of Life Sciences, Mokwon University, Taejon 302-729, Republic of Korea.
authors.forename: Dongmin
authors.initials: D
authors.lastname: Park
authors.forename: Michung
authors.initials: M
authors.lastname: Yoon
mesh_terms: D041721:3T3-L1 Cells; D017667:Adipocytes / Q000187:drug effects* / Q000378:metabolism; D050156:Adipogenesis / Q000187:drug effects* / Q000235:genetics; D000818:Animals; D022762:CCAAT-Enhancer-Binding Proteins / Q000037:antagonists & inhibitors / Q000235:genetics; D050556:Fatty Acid-Binding Proteins / Q000037:antagonists & inhibitors / Q000235:genetics; D016222:Fibroblast Growth Factor 2 / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D015870:Gene Expression / Q000187:drug effects; D036145:Ginsenosides / Q000494:pharmacology*; D050356:Lipid Metabolism / Q000187:drug effects; D061965:Matrix Metalloproteinase Inhibitors; D020782:Matrix Metalloproteinases / Q000235:genetics / Q000378:metabolism; D051379:Mice; D018919:Neovascularization, Physiologic / Q000187:drug effects* / Q000235:genetics; D047495:PPAR gamma / Q000037:antagonists & inhibitors / Q000235:genetics; D012333:RNA, Messenger / Q000037:antagonists & inhibitors / Q000096:biosynthesis; D019714:Tissue Inhibitor of Metalloproteinases / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000037:antagonists & inhibitors / Q000096:biosynthesis
chemical_list: D022762:CCAAT-Enhancer-Binding Proteins; D050556:Fatty Acid-Binding Proteins; D016222:Fibroblast Growth Factor 2; D036145:Ginsenosides; D061965:Matrix Metalloproteinase Inhibitors; D020782:Matrix Metalloproteinases; D047495:PPAR gamma; D012333:RNA, Messenger; D019714:Tissue Inhibitor of Metalloproteinases; D042461:Vascular Endothelial Growth Factor A; C530718:CEBPA protein, mouse; C493411:Fabp4 protein, mouse; C112772:ginsenoside compound K