Source:http://linkedlifedata.com/resource/pubmed/id/15932924
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
2005-8-17
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pubmed:abstractText |
Glucagon-like peptide-1(7-36NH2) (GLP-1) and peptide YY(3-36NH2) (PYY(3-36NH2)) are cosecreted from the intestine in response to nutrient ingestion. Peripheral administration of GLP-1 or PYY(3-36NH2) decreases food intake (FI) in rodents and humans; however, the exact mechanisms by which these peptides regulate FI remain unclear. Male C57BL/6 mice were injected (ip) with exendin-4(1-39) (Ex4, a GLP-1 receptor agonist) and/or PYY(3-36NH2) (0.03-3 microg), and FI was determined for up to 24 h. Ex4 and PYY(3-36NH2) alone decreased FI by up to 83 and 26%, respectively (P < 0.05-0.001), whereas a combination of the two peptides (0.06 microg Ex4 plus 3 microg PYY(3-36NH2)) further reduced FI for up to 8 h in a synergistic manner (P < 0.05-0.001). Ex4 and/or PYY(3-36NH2) delayed gastric emptying by a maximum of 19% (P < 0.01-0.001); however, there was no significant effect on locomotor activity nor was there induction of taste aversion. Capsaicin pretreatment prevented the inhibitory effect of Ex4 on FI (P < 0.05), but had no effect on the anorexigenic actions of PYY(3-36NH2). Similarly, exendin-4(9-39) (a GLP-1 receptor antagonist) partially abolished Ex4-induced anorexia (P < 0.05), but did not affect the satiation produced by PYY(3-36NH2). Conversely, BIIE0246 (a Y2 receptor antagonist) completely blocked the anorexigenic effects of PYY(3-36NH2) (P < 0.001), but had no effect on Ex4-induced satiety. Thus, Ex4 and PYY(3-36NH2) suppress FI via independent mechanisms involving a GLP-1 receptor-dependent, sensory afferent pathway (Ex4) and a Y2-receptor mediated pathway (PYY(3-36NH2)). These findings suggest that administration of low doses of Ex4 together with PYY(3-36NH2) may increase the suppression of FI without inducing significant side effects.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Peptide YY,
http://linkedlifedata.com/resource/pubmed/chemical/Peptides,
http://linkedlifedata.com/resource/pubmed/chemical/Venoms,
http://linkedlifedata.com/resource/pubmed/chemical/exenatide,
http://linkedlifedata.com/resource/pubmed/chemical/peptide YY (3-36)
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0013-7227
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
146
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3748-56
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:15932924-Animals,
pubmed-meshheading:15932924-Dose-Response Relationship, Drug,
pubmed-meshheading:15932924-Drug Synergism,
pubmed-meshheading:15932924-Eating,
pubmed-meshheading:15932924-Gastric Emptying,
pubmed-meshheading:15932924-Injections, Intraperitoneal,
pubmed-meshheading:15932924-Male,
pubmed-meshheading:15932924-Mice,
pubmed-meshheading:15932924-Mice, Inbred C57BL,
pubmed-meshheading:15932924-Obesity,
pubmed-meshheading:15932924-Peptide YY,
pubmed-meshheading:15932924-Peptides,
pubmed-meshheading:15932924-Satiety Response,
pubmed-meshheading:15932924-Venoms
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pubmed:year |
2005
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pubmed:articleTitle |
Peripheral exendin-4 and peptide YY(3-36) synergistically reduce food intake through different mechanisms in mice.
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pubmed:affiliation |
Department of Physiology, Room 3366, Medical Sciences Building, University of Toronto, 1 King's College Circle, Toronto, Ontario, Canada M5S 1A8.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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