Requirement of fibroblast growth factor 10 in development of white adipose tissue

  1. Hiroshi Sakaue1,5,
  2. Morichika Konishi2,5,
  3. Wataru Ogawa1,
  4. Toshiyuki Asaki2,
  5. Toshiyuki Mori1,
  6. Masahiro Yamasaki2,
  7. Masafumi Takata1,
  8. Hikaru Ueno3,
  9. Shigeaki Kato4,
  10. Masato Kasuga1,6, and
  11. Nobuyuki Itoh2,6
  1. 1Department of Clinical Molecular Medicine, Division of Diabetes, Digestive and Kidney Diseases, Kobe University Graduate School of Medicine, Chuo-ku, Kobe 650-0017, Japan; 2Department of Genetic Biochemistry, Kyoto University Graduate School of Pharmaceutical Sciences, Kyoto 606-8501, Japan; 3Department of Biochemistry and Molecular Physiology, University of Occupational and Environmental Health, School of Medicine, Kitakyushyu 807-8555, Japan; 4Institute of Molecular and Cellular Biosciences, University of Tokyo, Tokyo 113-0032, Japan

Abstract

Fibroblast growth factors (FGFs) are important intercellular signaling molecules in developmental processes. Here, we show that FGF10 is secreted by cultured preadipocytes and that prevention of FGF10 signaling inhibits the expression of C/EBPβ and the subsequent differentiation of these cells. An active form of C/EBPβ rescued differentiation of the cells in which FGF10 signaling was blocked. Development of white adipose tissue and the expression of C/EBPβ in this tissue of FGF10 knockout mice were markedly reduced, and the ability of embryonic fibroblasts derived from FGF10 knockout mice to differentiate into adipocytes was impaired. Therefore, FGF10 plays an important role in adipogenesis, at least partly by contributing to the expression of C/EBPβ through an autocrine/paracrine mechanism.

Keywords

Footnotes

  • 5 These authors contributed equally to this work.

  • 6 Corresponding authors.

  • E-MAIL kasuga{at}med.kobe-u.ac.jp; FAX 81-78-382-2080.

  • E-MAIL itohnobu{at}pharm.kyoto-u.ac.jp; FAX 81-75-753-4600.

  • Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.983202.

    • Received February 8, 2002.
    • Accepted March 1, 2002.
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