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The Mitogenic and Antiapoptotic Actions of Ghrelin in 3T3-L1 Adipocytes
Author(s) -
MinSeon Kim,
Cho Ya Yoon,
Pil Geum 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,
Kyong Soo Park
Publication year - 2004
Publication title -
molecular endocrinology
Language(s) - English
Resource type - Journals
eISSN - 1944-9917
pISSN - 0888-8809
DOI - 10.1210/me.2003-0459
Subject(s) - ghrelin , endocrinology , medicine , mapk/erk pathway , biology , adipocyte , irs1 , protein kinase b , 3t3 l1 , adipose tissue , growth hormone secretagogue receptor , cell growth , receptor , phosphatidylinositol , kinase , insulin receptor , signal transduction , microbiology and biotechnology , insulin , hormone , insulin resistance , biochemistry
Ghrelin, a stomach-derived hormone, induces adiposity when administered to rodents. Because 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 antiapoptotic effects of ghrelin. Ghrelin also stimulated the insulin receptor substrate-associated phosphatidylinositol 3-kinase/Akt pathway in 3T3-L1 preadipocytes and adipocytes, whereas inhibition of this pathway blocked the effects of ghrelin on cell proliferation, antiapoptosis 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 phosphatidylinositol 3-kinase/Akt pathways.

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