지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2013.1
- 수록면
- 141 - 147 (7page)
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초록· 키워드
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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-phosphate-activated 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 ${\gamma}$ ($PPAR{\gamma}$) 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 $PPAR{\gamma}$ 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 $PPAR{\gamma}$. The modulating effect of CK on expression of genes involved in lipogenesis was abrogated in part by treatment with troglitazone, a $PPAR{\gamma}$ agonist. CK significantly decreased accumulation of lipid droplets and $PPAR{\gamma}$ expression induced by troglitazone in 3T3-L1 adipocytes, suggesting that CK down-regulates $PPAR{\gamma}$ expression and its transcriptional activity as well as abrogates $PPAR{\gamma}$ signaling pathway induced by troglitazone, a $PPAR{\gamma}$ agonist. These results indicate that CK inhibits 3T3-L1 adipogenic differentiation by inhibiting $PPAR{\gamma}$ and FAS expressions as well as interferes with $PPAR{\gamma}$ signaling pathway induced by $PPAR{\gamma}$ agonist, and may act as an anti-adipogenic ginsenoside for regulating body fat through its effects on differentiation.
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