Source:http://linkedlifedata.com/resource/pubmed/id/15845619
Switch to
Predicate | Object |
---|---|
rdf:type | |
lifeskim:mentions | |
pubmed:issue |
8
|
pubmed:dateCreated |
2005-7-12
|
pubmed:abstractText |
Relaxin-3 (INSL-7) is a recently discovered member of the insulin superfamily. Relaxin-3 mRNA is expressed in the nucleus incertus of the brainstem, which has projections to the hypothalamus. Relaxin-3 binds with high affinity to the LGR7 receptor and to the previously orphan G protein-coupled receptor GPCR135. GPCR135 mRNA is expressed predominantly in the central nervous system, particularly in the paraventricular nucleus (PVN). The presence of relaxin-3 and these receptors in the PVN led us to investigate the effect of central administration of relaxin-3 on food intake in male Wistar rats. The receptor involved in mediating these effects was also investigated. Intracerebroventricular injections of human relaxin-3 (H3) to satiated rats significantly increased food intake 1 h post administration in the early light phase [0.96 +/- 0.16 g (vehicle) vs. 1.81 +/- 0.21 g (180 pmol H3), P < 0.05] and the early dark phase [2.95 +/- 0.45 g (vehicle) vs. 4.39 +/- 0.39 g (180 pmol H3), P < 0.05]. Intra-PVN H3 administration significantly increased 1-h food intake in satiated rats in the early light phase [0.34 +/- 0.16 g (vehicle) vs. 1.23 +/- 0.30 g (18 pmol H3), P < 0.05] and the early dark phase [4.43 +/- 0.32 g (vehicle) vs. 6.57 +/- 0.42 g (18 pmol H3), P < 0.05]. Feeding behavior increased after intra-PVN H3. Equimolar doses of human relaxin-2, which binds the LGR7 receptor but not GPCR135, did not increase feeding. Hypothalamic neuropeptide Y, proopiomelanocortin, or agouti-related peptide mRNA expression did not change after acute intracerebroventricular H3. These results suggest a novel role for relaxin-3 in appetite regulation.
|
pubmed:language |
eng
|
pubmed:journal | |
pubmed:citationSubset |
AIM
|
pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Neuropeptide Y,
http://linkedlifedata.com/resource/pubmed/chemical/Pro-Opiomelanocortin,
http://linkedlifedata.com/resource/pubmed/chemical/RLN3 protein, human,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Relaxin
|
pubmed:status |
MEDLINE
|
pubmed:month |
Aug
|
pubmed:issn |
0013-7227
|
pubmed:author | |
pubmed:issnType |
Print
|
pubmed:volume |
146
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
3295-300
|
pubmed:dateRevised |
2006-11-15
|
pubmed:meshHeading |
pubmed-meshheading:15845619-Animals,
pubmed-meshheading:15845619-Cerebral Ventricles,
pubmed-meshheading:15845619-Gene Expression Regulation,
pubmed-meshheading:15845619-Hyperphagia,
pubmed-meshheading:15845619-Hypothalamus,
pubmed-meshheading:15845619-Injections, Intraventricular,
pubmed-meshheading:15845619-Male,
pubmed-meshheading:15845619-Midline Thalamic Nuclei,
pubmed-meshheading:15845619-Neuropeptide Y,
pubmed-meshheading:15845619-Pro-Opiomelanocortin,
pubmed-meshheading:15845619-RNA, Messenger,
pubmed-meshheading:15845619-Rats,
pubmed-meshheading:15845619-Rats, Wistar,
pubmed-meshheading:15845619-Relaxin
|
pubmed:year |
2005
|
pubmed:articleTitle |
Central relaxin-3 administration causes hyperphagia in male Wistar rats.
|
pubmed:affiliation |
Endocrine Unit, Imperial College School of Medicine, Hammersmith Hospital, London W12 ONN, United Kingdom.
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|