Source:http://linkedlifedata.com/resource/pubmed/id/21525005
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
24
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pubmed:dateCreated |
2011-6-13
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pubmed:abstractText |
The activation of renin-angiotensin system contributes to the development of metabolic syndrome and diabetes as well as hypertension. However, it remains undetermined how renin-angiotensin system is implicated in feeding behavior. Here, we show that angiotensin II type 1 (AT(1)) receptor signaling regulates the hypothalamic neurocircuit that is involved in the control of food intake. Compared with wild-type Agtr1a(+/+) mice, AT(1) receptor knock-out (Agtr1a(-/-)) mice were hyperphagic and obese with increased adiposity on an ad libitum diet, whereas Agtr1a(-/-) mice were lean with decreased adiposity on a pair-fed diet. In the hypothalamus, mRNA levels of anorexigenic neuropeptide corticotropin-releasing hormone (Crh) were lower in Agtr1a(-/-) mice than in Agtr1a(+/+) mice both on an ad libitum and pair-fed diet. Furthermore, intracerebroventricular administration of CRH suppressed food intake both in Agtr1a(+/+) and Agtr1a(-/-) mice. In addition, the Crh gene promoter was significantly transactivated via the cAMP-responsive element by angiotensin II stimulation. These results thus demonstrate that central AT(1) receptor signaling plays a homeostatic role in the regulation of food intake by maintaining gene expression of Crh in hypothalamus and suggest a therapeutic potential of central AT(1) receptor blockade in feeding disorders.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Corticotropin-Releasing Hormone,
http://linkedlifedata.com/resource/pubmed/chemical/Neuropeptides,
http://linkedlifedata.com/resource/pubmed/chemical/Oligopeptides,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrrolidonecarboxylic Acid,
http://linkedlifedata.com/resource/pubmed/chemical/Receptor, Angiotensin, Type 1,
http://linkedlifedata.com/resource/pubmed/chemical/pyroglutamyl-histidyl-glycine
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
1083-351X
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pubmed:author | |
pubmed:issnType |
Electronic
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pubmed:day |
17
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pubmed:volume |
286
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
21458-65
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pubmed:meshHeading |
pubmed-meshheading:21525005-Adipose Tissue,
pubmed-meshheading:21525005-Animals,
pubmed-meshheading:21525005-Corticotropin-Releasing Hormone,
pubmed-meshheading:21525005-Feeding Behavior,
pubmed-meshheading:21525005-Gene Expression Regulation,
pubmed-meshheading:21525005-HEK293 Cells,
pubmed-meshheading:21525005-Humans,
pubmed-meshheading:21525005-Hypothalamus,
pubmed-meshheading:21525005-Male,
pubmed-meshheading:21525005-Mice,
pubmed-meshheading:21525005-Mice, Knockout,
pubmed-meshheading:21525005-Neuropeptides,
pubmed-meshheading:21525005-Obesity,
pubmed-meshheading:21525005-Oligopeptides,
pubmed-meshheading:21525005-Pyrrolidonecarboxylic Acid,
pubmed-meshheading:21525005-Receptor, Angiotensin, Type 1
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pubmed:year |
2011
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pubmed:articleTitle |
Angiotensin II type 1 receptor signaling regulates feeding behavior through anorexigenic corticotropin-releasing hormone in hypothalamus.
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pubmed:affiliation |
Department of Cardiovascular Science and Medicine, Chiba University Graduate School of Medicine, Chiba, Chiba 260-8670, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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