Horm Metab Res 2009; 41(4): 271-276
DOI: 10.1055/s-0028-1103277
Original Basic

© Georg Thieme Verlag KG Stuttgart · New York

Increase of Adipogenesis by Ginsenoside (Rh2) in 3T3-L1 Cell via an Activation of Glucocorticoid Receptor

C-S. Niu 1 [*] , C-H. Yeh 2 [*] , M-F. Yeh 1 , J-T. Cheng 2 , 3
  • 1Department of Nursing, Tzu Chi College of Technology, Hualien, Taiwan
  • 2Institute of Basic Medical Sciences and College of Medicine, National Cheng Kung University, Tainan City, Taiwan
  • 3Department of Pharmacology, College of Medicine, National Cheng Kung University, Tainan City, Taiwan
Further Information

Publication History

received 10.09.2008

accepted 30.10.2008

Publication Date:
01 December 2008 (online)

Abstract

Adipocyte plays an important role in lipid regulation in mammals. Understanding of adipocyte differentiation becomes a key issue for the development of anti-obesity agent. Glucocorticoids (GCs) regulate lipid metabolism through promoting lipogenesis in adipose tissue. Ginsenoside Rh2, with a similar chemical structure as GCs, shows antidiabetic, anti-inflammatory, and anticancer actions both in vivo and in vitro. However, effect of Rh2 on glucocorticoid receptor (GR) for an increase of adipogenesis like GCs remains unclear. In the present study, we employed ginsenoside Rh2 to investigate the changes in adipogenetic process of 3T3-L1, one of the widely used preadipocytes, through activating GR or not. In leuciferase assay, we found that ginsenoside Rh2 induced GRs transitivity in a way as dexamethasone, which was deleted by RU486 at concentrations sufficient to block GR. Moreover, 3T3-L1 preadipocytes were differentiated into adipocytes by adipogenic induction medium containing 0.01 to 1 μM of ginsenoside Rh2. Also, RU486 blocked this adipogenesis induced by ginsenoside Rh2 or dexamethasone. The obtained results suggest that ginsenoside Rh2 can promote preadipocytes differentiation through activating GR. This finding seems helpful for the understanding of ginsenosides in the regulation of lipid metabolism.

References

1 These authors contributed equally to this work.

Correspondence

Prof. J-T. Cheng

Department of Pharmacology

College of Medicine

National Cheng Kung University

Tainan City

70101 Taiwan

Phone: +886/6/331 85 16

Fax: +886/6/238 65 48

Email: [email protected]