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

    Research output: Contribution to journalArticle

    249 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

    Fingerprint

    Obesity
    Bombesin
    Bombesin Receptors
    Hyperphagia
    Peptide Receptors
    Adiposity
    Muscle Contraction
    G-Protein-Coupled Receptors
    Energy Metabolism
    Smooth Muscle
    Gastrointestinal Tract
    bombesin receptor subtype 3
    Central Nervous System
    Ligands
    Hypertension
    Glucose
    Peptides

    ASJC Scopus subject areas

    • General

    Cite this

    Ohki-Hamazaki, H., Watase, K., Yamamoto, K., Ogura, H., Yamano, M., Yamada, K., ... 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

    Mice lacking bombesin receptor subtype-3 develop metabolic defects and obesity. / Ohki-Hamazaki, Hiroko; Watase, Kei; Yamamoto, Kazutoshi; Ogura, Hiroo; Yamano, Mariko; Yamada, Kazuyuki; Maeno, Hiroshi; Imaki, Junko; Kikuyama, Sakae; Wada, Etsuko; Wada, Keiji.

    In: Nature, Vol. 390, No. 6656, 13.11.1997, p. 165-169.

    Research output: Contribution to journalArticle

    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, vol. 390, no. 6656, pp. 165-169. https://doi.org/10.1038/36568
    Ohki-Hamazaki H, Watase K, Yamamoto K, Ogura H, Yamano M, Yamada K et al. Mice lacking bombesin receptor subtype-3 develop metabolic defects and obesity. Nature. 1997 Nov 13;390(6656):165-169. https://doi.org/10.1038/36568
    Ohki-Hamazaki, Hiroko ; Watase, Kei ; Yamamoto, Kazutoshi ; Ogura, Hiroo ; Yamano, Mariko ; Yamada, Kazuyuki ; Maeno, Hiroshi ; Imaki, Junko ; Kikuyama, Sakae ; Wada, Etsuko ; Wada, Keiji. / Mice lacking bombesin receptor subtype-3 develop metabolic defects and obesity. In: Nature. 1997 ; Vol. 390, No. 6656. pp. 165-169.
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