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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
6656
|
| pubmed:dateCreated |
1997-11-25
|
| pubmed: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.
|
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Hormones,
http://linkedlifedata.com/resource/pubmed/chemical/Leptin,
http://linkedlifedata.com/resource/pubmed/chemical/Proteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Bombesin,
http://linkedlifedata.com/resource/pubmed/chemical/bombesin receptor subtype 3
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Nov
|
| pubmed:issn |
0028-0836
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
13
|
| pubmed:volume |
390
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
165-9
|
| pubmed:dateRevised |
2006-11-15
|
| pubmed:meshHeading |
pubmed-meshheading:9367152-Adipose Tissue, Brown,
pubmed-meshheading:9367152-Animals,
pubmed-meshheading:9367152-Blood Pressure,
pubmed-meshheading:9367152-Body Weight,
pubmed-meshheading:9367152-Energy Metabolism,
pubmed-meshheading:9367152-Female,
pubmed-meshheading:9367152-Gene Deletion,
pubmed-meshheading:9367152-Gene Targeting,
pubmed-meshheading:9367152-Glucose,
pubmed-meshheading:9367152-Glucose Tolerance Test,
pubmed-meshheading:9367152-Heart Rate,
pubmed-meshheading:9367152-Hormones,
pubmed-meshheading:9367152-Leptin,
pubmed-meshheading:9367152-Male,
pubmed-meshheading:9367152-Metabolic Diseases,
pubmed-meshheading:9367152-Mice,
pubmed-meshheading:9367152-Mice, Inbred ICR,
pubmed-meshheading:9367152-Motor Activity,
pubmed-meshheading:9367152-Obesity,
pubmed-meshheading:9367152-Proteins,
pubmed-meshheading:9367152-Receptors, Bombesin
|
| pubmed:year |
1997
|
| pubmed:articleTitle |
Mice lacking bombesin receptor subtype-3 develop metabolic defects and obesity.
|
| pubmed:affiliation |
Department of Degenerative Neurological Diseases, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan. hamazaki@prit.go.jp
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|