Compound K attenuates lipid accumulation through down-regulation of peroxisome proliferator-activated receptor γ in 3T3-L1 cells

• Published in: Applied biological chemistry 2013, 56(2), , pp.141-147
• Main Authors: Lee, Dong Hun, Jeong-Woo, Kang, Yong-Seok, Song, Jung-Hee, Kim, Kim, Man Sub, Bak Yesol, Oh Deok-Kun, Do-Young, Yoon
• Format: Article
• Language: English
• Subjects: Accumulation; Adenosine; Adenosine kinase; Adipocytes; Agonists; Body fat; Cell activation; Cell differentiation; Diabetes mellitus; Differentiation; Down-regulation; Fatty acids; Fatty-acid synthase; Gene expression; Ginseng; Ginsenosides; Hepatoma; Kinases; Lipids; Lipogenesis; Low concentrations; Obesity; Protein kinase; Receptors; Signal transduction; Signaling; Transcription; Troglitazone; 농학
• ISSN: 2468-0834; 2468-0842
• DOI: 10.1007/s13765-012-3270-3

Compound K (CK) is rare ginsenosides present at low concentrations or absent in ginseng roots. These rare ginsenosides can be produced from the major ginsenosides Rb1, Rb2, and Rd through hydrolysis of sugar moieties. Recently, CK has been found to have anti-diabetic effects through adenosine 5-phosphateactivated protein kinase (AMPK) activation in human hepatoma cells and a stimulatory effect of glucose uptake in 3T3-L1 adipocytes, as well as anti-obesity effect by down regulation of peroxisome proliferator-activated receptor γ (PPARγ) gene expression in 3T3-L1. However, detailed anti-obesity pathway by CK remains unclear. In the present study, the effects of CK produced from Sulfolobus acidocaldarius on PPARγ signaling during adipocyte differentiation in 3T3-L1 cell were examined. Treatment of differentiating 3T3-L1 cells with CK resulted in down-regulation of fatty acid synthase (FAS), a target gene of PPARγ. The modulating effect of CK on expression of genes involved in lipogenesis was abrogated in part by treatment with troglitazone, a PPARγ agonist. CK significantly decreased accumulation of lipid droplets and PPARγ expression induced by troglitazone in 3T3-L1 adipocytes, suggesting that CK downregulates PPARγ expression and its transcriptional activity as well as abrogates PPARγ signaling pathway induced by troglitazone, a PPARγ agonist. These results indicate that CK inhibits 3T3-L1 adipogenic differentiation by inhibiting PPARγ and FAS expressions as well as interferes with PPARγ signaling pathway induced by PPARγ agonist, and may act as an anti-adipogenic ginsenoside for regulating body fat through its effects on differentiation.