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Mice lacking bombesin receptor subtype-3 develop metabolic defects and obesity
H Ohki-Hamazaki1, K Watase, K Yamamoto
1Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan. hamazaki@prit.go.jp
Nature
|November 21, 1997
Summary
Mice lacking the bombesin receptor subtype-3 (BRS-3) developed obesity, hypertension, and impaired glucose metabolism, indicating BRS-3
Area of Science:
- Endocrinology
- Metabolism
- Neuroscience
Background:
- Mammalian bombesin-like peptides regulate physiological processes via G-protein-coupled receptors.
- Key receptors include gastrin-releasing peptide receptor (GRP-R), neuromedin B receptor (NMB-R), and bombesin receptor subtype-3 (BRS-3).
- The in vivo function of BRS-3 remains unclear due to its low affinity and lack of a natural ligand.
Purpose of the Study:
- To determine the in vivo function of bombesin receptor subtype-3 (BRS-3).
- To investigate the role of BRS-3 in regulating metabolism and energy balance.
- To establish a BRS-3-deficient mouse model for studying obesity and related diseases.
Main Methods:
- Generation of BRS-3-deficient mice.
- Phenotypic analysis of BRS-3 deficient mice, including metabolic rate, feeding efficiency, and glucose metabolism.
- Assessment of obesity, hypertension, and adiposity in the knockout model.
Main Results:
- BRS-3 deficient mice exhibited mild obesity, hypertension, and impaired glucose metabolism.
- These mice showed a reduced metabolic rate, increased feeding efficiency, and hyperphagia.
- Data indicates BRS-3 is crucial for regulating endocrine processes, metabolism, energy balance, and adiposity.
Conclusions:
- Bombesin receptor subtype-3 (BRS-3) plays a significant role in regulating energy homeostasis.
- BRS-3 deficiency leads to metabolic dysfunction and obesity.
- BRS-3 deficient mice represent a valuable model for investigating human obesity and associated metabolic disorders.