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This version published online on June 3, 2004
Molecular Endocrinology, doi:10.1210/me.2003-0459
A more recent version of this article appeared on September 1, 2004
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Submitted on December 2, 2003
Accepted on May 25, 2004

The mitogenic and anti-apoptotic actions of ghrelin in 3T3-L1 adipocytes

Min Seon Kim, Cho Ya Yoon, Phil Gum Jang, Young Joo Park, Chan Soo Shin, Hye Sun Park, Je Won Ryu, Youngmi Kim Pak, Joong Yeol Park, Ki Up Lee, Seong Yeon Kim, Hong Kyu Lee, Young Bum Kim, and Kyong Soo Park*

Department of Internal Medicine, Seoul National University College of Medicine, Seoul, Korea; Department of Internal Medicine and Asan Institute for Life Sciences, University of Ulsan College of Medicine, Seoul, Korea; Medicine-Endocrine, Beth Israel Deacioness Medical Center Harvard Medical School, Boston, USA

* To whom correspondence should be addressed. E-mail: kspark{at}snu.ac.kr.

Ghrelin, a stomach-derived hormone, induces adiposity when administered to rodents. Since ghrelin receptor is abundantly expressed in adipose tissue, we investigated the role of ghrelin in adipocyte biology. We observed ghrelin receptor expression in 3T3-L1 preadipocytes and adipocytes. Treatment of preadipocytes with ghrelin induced cellular proliferation and differentiation to mature adipocytes, as well as basal and insulin stimulated glucose transport, but it inhibited adipocyte apoptosis induced by serum deprivation. Exposure of 3T3-L1 cells to ghrelin caused a rapid activation of MAPKs, especially ERK1/2. Chemical inhibition of MAPK blocked the mitogenic and anti-apoptotic effects of ghrelin. Ghrelin also stimulated the insulin receptor substrate (IRS-1) associated phosphatidylinositol 3-kinase (PI3K)/Akt pathway in 3T3-L1 preadipocytes and adipocytes, whereas inhibition of this pathway blocked the effects of ghrelin on cell proliferation, anti-apoptosis and glucose uptake.

These findings suggest that the direct effects of ghrelin on proliferation, differentiation and apoptosis in adipocytes may play a role in regulating fat cell number. These effects may be mediated via activation of the MAPK and PI3K/Akt pathways.
Key words: ghrelin • adipocytes • proliferation • differentiation • anti-apoptosis • MAP kinase • PI3 kinase




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