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dc.contributor.authorWynick, D.en_US
dc.contributor.authorWeinshenker, Daviden_US
dc.contributor.authorSteiner, Robert A.en_US
dc.contributor.authorClifton, Donald K.en_US
dc.contributor.authorHohmann, John G.en_US
dc.contributor.authorTeklemichael, Dawit N.en_US
dc.date.accessioned2008-10-17T20:40:23Z
dc.date.available2008-10-17T20:40:23Z
dc.date.issued2004-04en_US
dc.identifier.citationMol Cell Biol. 2004 Apr;24(7):2978-85en_US
dc.identifier.urihttp://hdl.handle.net/1773/4303
dc.description.abstractNeuropeptide Y (NPY) and galanin have both been implicated in the regulation of body weight, yet mice bearing deletions of either of these molecules have unremarkable metabolic phenotypes. To investigate whether galanin and NPY might compensate for one another, we produced mutants lacking both neuropeptides (GAL(-/-)/NPY(-/-)). We found that male GAL(-/-)/NPY(-/-) mice ate significantly more and were much heavier (30%) than wild-type (WT) controls. GAL(-/-)/NPY(-/-) mice responded to a high-fat diet by gaining more weight than WT mice gain, and they were unable to regulate their weight normally after a change in diet. GAL(-/-)/NPY(-/-) mice had elevated levels of leptin, insulin, and glucose, and they lost more weight than WT mice during chronic leptin treatment. Galanin mRNA was increased in the hypothalamus of NPY(-/-) mice, providing evidence of compensatory regulation in single mutants. The disruption of energy balance observed in GAL(-/-)/NPY(-/-) double knockouts is not found in the phenotype of single knockouts of either molecule. The unexpected obesity phenotype may result from the dysregulation of the leptin and insulin systems that normally keep body weight within the homeostatic range.en_US
dc.language.isoen_USen_US
dc.publisherAmerican Society for Microbiologyen_US
dc.subjectneuropeptide Yen_US
dc.subjectgalaninen_US
dc.subjectbody weighten_US
dc.subjectmiceen_US
dc.subject.meshNeuropeptide Y, genetics, metabolismen_US
dc.subject.meshBody Weighten_US
dc.subject.meshEatingen_US
dc.subject.meshDietary Fatsen_US
dc.subject.meshMice, Inbred Strainsen_US
dc.subject.meshGalanin, genetics, metabolismen_US
dc.subject.meshEndocrine System, physiopathologyen_US
dc.subject.meshMice, Knockouten_US
dc.subject.meshHormones, blooden_US
dc.subject.meshDorsomedial Hypothalamic Nucleus, cytology, metabolismen_US
dc.subject.meshMiceen_US
dc.subject.meshCircadian Rhythmen_US
dc.subject.meshInsulin, metabolismen_US
dc.subject.meshLeptin, administration & dosage, metabolismen_US
dc.subject.meshAnimalsen_US
dc.subject.meshMotor Activity, physiologyen_US
dc.subject.meshObesity, genetics, metabolismen_US
dc.subject.meshResearch Support, U.S. Gov't, P.H.S.en_US
dc.subject.meshPhenotypeen_US
dc.subject.meshResearch Support, Non-U.S. Gov'ten_US
dc.subject.meshResearch Support, U.S. Gov't, Non-P.H.S.en_US
dc.subject.meshMaleen_US
dc.titleObesity and endocrine dysfunction in mice with deletions of both neuropeptide Y and galaninen_US
dc.typeArticleen_US


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