| pubmed-article:16484325 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:16484325 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:16484325 | lifeskim:mentions | umls-concept:C0026809 | lld:lifeskim |
| pubmed-article:16484325 | lifeskim:mentions | umls-concept:C0020505 | lld:lifeskim |
| pubmed-article:16484325 | lifeskim:mentions | umls-concept:C0911014 | lld:lifeskim |
| pubmed-article:16484325 | lifeskim:mentions | umls-concept:C0011847 | lld:lifeskim |
| pubmed-article:16484325 | lifeskim:mentions | umls-concept:C0205227 | lld:lifeskim |
| pubmed-article:16484325 | pubmed:issue | 6 | lld:pubmed |
| pubmed-article:16484325 | pubmed:dateCreated | 2006-5-18 | lld:pubmed |
| pubmed-article:16484325 | pubmed:abstractText | Ghrelin is an orexigenic peptide involved in the regulation of energy homeostasis. To investigate the role of ghrelin in the hyperphagia associated with uncontrolled streptozotocin-induced diabetes, food intake was followed in diabetic ghrelin knockout (ghrelin(-/-)) and control wild-type (ghrelin(+/+)) mice and diabetic Naval Medical Research Institute noninbred Swiss mice treated with either saline or the ghrelin receptor antagonist, D-Lys3-GH-releasing peptide-6 (D-Lys3-GHRP-6) for 5 d. In diabetic ghrelin(-/-) mice, hyperphagia was attenuated, and the maximal increase in food intake was 50% lower in mutant than in wild-type mice. The increased food intake observed during the light period (1000-1200 h) in ghrelin(+/+) mice was abolished in mutant mice. Diabetic ghrelin(-/-) mice lost 12.4% more body weight than ghrelin(+/+) mice. In diabetic ghrelin(+/+) mice, but not in ghrelin(-/-) mice, the number of neuropeptide Y (NPY)-immunoreactive neurons was significantly increased. Diabetic Naval Medical Research Institute noninbred Swiss mice were hyperphagic and had increased plasma ghrelin levels. Treatment with D-Lys3-GHRP-6 reduced daily food intake by 23% and reversed the increased food intake observed during the light period. The change in the number of NPY- (2.4-fold increase) and alpha-MSH (1.7-fold decrease)-immunoreactive hypothalamic neurons induced by diabetes was normalized by D-Lys3-GHRP-6 treatment. Our results suggest that enhanced NPY and reduced alpha-MSH expression are secondary to the release of ghrelin, which should be considered the underlying trigger of hyperphagia associated with uncontrolled diabetes. | lld:pubmed |
| pubmed-article:16484325 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16484325 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16484325 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16484325 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:16484325 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16484325 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:16484325 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16484325 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16484325 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16484325 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16484325 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16484325 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16484325 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16484325 | pubmed:month | Jun | lld:pubmed |
| pubmed-article:16484325 | pubmed:issn | 0013-7227 | lld:pubmed |
| pubmed-article:16484325 | pubmed:author | pubmed-author:PeetersT LTL | lld:pubmed |
| pubmed-article:16484325 | pubmed:author | pubmed-author:TaniCC | lld:pubmed |
| pubmed-article:16484325 | pubmed:author | pubmed-author:DelporteCC | lld:pubmed |
| pubmed-article:16484325 | pubmed:author | pubmed-author:DongJJ | lld:pubmed |
| pubmed-article:16484325 | pubmed:author | pubmed-author:DepoortereII | lld:pubmed |
| pubmed-article:16484325 | pubmed:author | pubmed-author:De SmetBB | lld:pubmed |
| pubmed-article:16484325 | pubmed:author | pubmed-author:MoecharsDD | lld:pubmed |
| pubmed-article:16484325 | pubmed:author | pubmed-author:CoulieBB | lld:pubmed |
| pubmed-article:16484325 | pubmed:author | pubmed-author:Vanden... | lld:pubmed |
| pubmed-article:16484325 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16484325 | pubmed:volume | 147 | lld:pubmed |
| pubmed-article:16484325 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16484325 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16484325 | pubmed:pagination | 2634-42 | lld:pubmed |
| pubmed-article:16484325 | pubmed:dateRevised | 2007-11-15 | lld:pubmed |
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| pubmed-article:16484325 | pubmed:meshHeading | pubmed-meshheading:16484325... | lld:pubmed |
| pubmed-article:16484325 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16484325 | pubmed:articleTitle | Role of endogenous ghrelin in the hyperphagia of mice with streptozotocin-induced diabetes. | lld:pubmed |
| pubmed-article:16484325 | pubmed:affiliation | Center for Gastroenterological Research, Catholitic University of Leuven, 3000 Leuven, Belgium. | lld:pubmed |
| pubmed-article:16484325 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16484325 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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| http://linkedlifedata.com/r... | pubmed:referesTo | pubmed-article:16484325 | lld:pubmed |
