Source:http://linkedlifedata.com/resource/pubmed/id/16484325
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2006-5-18
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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.
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pubmed:commentsCorrections | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Blood Glucose,
http://linkedlifedata.com/resource/pubmed/chemical/Ghrelin,
http://linkedlifedata.com/resource/pubmed/chemical/Glucagon,
http://linkedlifedata.com/resource/pubmed/chemical/Neuropeptide Y,
http://linkedlifedata.com/resource/pubmed/chemical/Oligopeptides,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Hormones,
http://linkedlifedata.com/resource/pubmed/chemical/Streptozocin,
http://linkedlifedata.com/resource/pubmed/chemical/alpha-MSH,
http://linkedlifedata.com/resource/pubmed/chemical/growth hormone releasing hexapeptide
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pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0013-7227
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
147
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2634-42
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:16484325-Animals,
pubmed-meshheading:16484325-Arcuate Nucleus,
pubmed-meshheading:16484325-Blood Glucose,
pubmed-meshheading:16484325-Body Weight,
pubmed-meshheading:16484325-Diabetes Mellitus, Experimental,
pubmed-meshheading:16484325-Ghrelin,
pubmed-meshheading:16484325-Glucagon,
pubmed-meshheading:16484325-Hyperphagia,
pubmed-meshheading:16484325-Male,
pubmed-meshheading:16484325-Mice,
pubmed-meshheading:16484325-Mice, Inbred C57BL,
pubmed-meshheading:16484325-Neuropeptide Y,
pubmed-meshheading:16484325-Oligopeptides,
pubmed-meshheading:16484325-Peptide Hormones,
pubmed-meshheading:16484325-Streptozocin,
pubmed-meshheading:16484325-alpha-MSH
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pubmed:year |
2006
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pubmed:articleTitle |
Role of endogenous ghrelin in the hyperphagia of mice with streptozotocin-induced diabetes.
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pubmed:affiliation |
Center for Gastroenterological Research, Catholitic University of Leuven, 3000 Leuven, Belgium.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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