Mice lacking bombesin receptor subtype-3 develop metabolic defects and obesity

Hiroko Ohki-Hamazaki*, Kei Watase, Kazutoshi Yamamoto, Hiroo Ogura, Mariko Yamano, Kazuyuki Yamada, Hiroshi Maeno, Junko Imaki, Sakae Kikuyama, Etsuko Wada, Keiji Wada

*この研究の対応する著者

    研究成果: Article査読

    271 被引用数 (Scopus)

    抄録

    Mammalian bombesin-like peptides are widely distributed in the central nervous system as well as in the gastrointestinal tract, where they modulate smooth-muscle contraction, exocrine and endocrine processes, metabolism and behaviour. They bind to G-protein-coupled receptors on the cell surface to elicit their effects. Bombesin-like peptide receptors cloned so far include, gastrin-releasing peptide receptor (GRP-R), neuromedin B receptor (NMB-R), and bombesin receptor subtype-3 (BRS-3). However, despite the molecular characterization of BRS-3, determination of its function has been difficult as a result of its low affinity for bombesin and its lack of an identified natural ligand. We have generated BRS-3-deficient mice in an attempt to determine the in vivo function of the receptor. Mice lacking functional BRS- 3 developed a mild obesity, associated with hypertension and impairment of glucose metabolism. They also exhibited reduced metabolic rate, increased feeding efficiency and subsequent hyperphagia. Our data suggest that BRS-3 is required for the regulation of endocrine processes and metabolism responsible for energy balance and adiposity. BRS-3-deficient mice provide a useful new model for the investigation of human obesity and associated diseases.

    本文言語English
    ページ(範囲)165-169
    ページ数5
    ジャーナルNature
    390
    6656
    DOI
    出版ステータスPublished - 1997 11月 13

    ASJC Scopus subject areas

    • 一般

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