| First Author | Ohki-Hamazaki H | Year | 1997 |
| Journal | Nature | Volume | 390 |
| Issue | 6656 | Pages | 165-9 |
| PubMed ID | 9367152 | Mgi Jnum | J:44242 |
| Mgi Id | MGI:1099616 | Doi | 10.1038/36568 |
| Citation | Ohki-Hamazaki H, et al. (1997) Mice lacking bombesin receptor subtype-3 develop metabolic defects and obesity. Nature 390(6656):165-9 |
| abstractText | 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. |
