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 and Keiji Wada ()
Additional contact information
Hiroko Ohki-Hamazaki: National Institute of Neuroscience, National Center of Neurology and Psychiatry
Kei Watase: National Institute of Neuroscience, National Center of Neurology and Psychiatry
Kazutoshi Yamamoto: School of Education, Waseda University
Hiroo Ogura: Tsukuba Research Laboratories, Eisai Co. Ltd.
Mariko Yamano: Osaka Prefectural College of Health Sciences
Kazuyuki Yamada: National Institute of Neuroscience, National Center of Neurology and Psychiatry
Hiroshi Maeno: National Institute of Neuroscience, National Center of Neurology and Psychiatry
Junko Imaki: Nippon Medical School
Sakae Kikuyama: School of Education, Waseda University
Etsuko Wada: National Institute of Neuroscience, National Center of Neurology and Psychiatry
Keiji Wada: National Institute of Neuroscience, National Center of Neurology and Psychiatry

Nature, 1997, vol. 390, issue 6656, 165-169

Abstract: 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 behaviour1. 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)2,3, neuromedin B receptor (NMB-R)4,5, and bombesin receptor subtype-3 (BRS-3)6,7. 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.

Date: 1997
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DOI: 10.1038/36568

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