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

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    255 Citations (Scopus)

    Abstract

    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.

    Original languageEnglish
    Pages (from-to)165-169
    Number of pages5
    JournalNature
    Volume390
    Issue number6656
    DOIs
    Publication statusPublished - 1997 Nov 13

    ASJC Scopus subject areas

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    Ohki-Hamazaki, H., Watase, K., Yamamoto, K., Ogura, H., Yamano, M., Yamada, K., Maeno, H., Imaki, J., Kikuyama, S., Wada, E., & Wada, K. (1997). Mice lacking bombesin receptor subtype-3 develop metabolic defects and obesity. Nature, 390(6656), 165-169. https://doi.org/10.1038/36568