Obesity and endocrine dysfunction in mice with deletions of both neuropeptide Y and galanin

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Obesity and endocrine dysfunction in mice with deletions of both neuropeptide Y and galanin

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dc.contributor.author Wynick, D. en_US
dc.contributor.author Weinshenker, David en_US
dc.contributor.author Steiner, Robert A. en_US
dc.contributor.author Clifton, Donald K. en_US
dc.contributor.author Hohmann, John G. en_US
dc.contributor.author Teklemichael, Dawit N. en_US
dc.date.accessioned 2008-10-17T20:40:23Z
dc.date.available 2008-10-17T20:40:23Z
dc.date.issued 2004-04 en_US
dc.identifier.citation Mol Cell Biol. 2004 Apr;24(7):2978-85 en_US
dc.identifier.uri http://hdl.handle.net/1773/4303
dc.description.abstract Neuropeptide 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.iso en_US en_US
dc.publisher American Society for Microbiology en_US
dc.subject neuropeptide Y en_US
dc.subject galanin en_US
dc.subject body weight en_US
dc.subject mice en_US
dc.subject.mesh Neuropeptide Y, genetics, metabolism en_US
dc.subject.mesh Body Weight en_US
dc.subject.mesh Eating en_US
dc.subject.mesh Dietary Fats en_US
dc.subject.mesh Mice, Inbred Strains en_US
dc.subject.mesh Galanin, genetics, metabolism en_US
dc.subject.mesh Endocrine System, physiopathology en_US
dc.subject.mesh Mice, Knockout en_US
dc.subject.mesh Hormones, blood en_US
dc.subject.mesh Dorsomedial Hypothalamic Nucleus, cytology, metabolism en_US
dc.subject.mesh Mice en_US
dc.subject.mesh Circadian Rhythm en_US
dc.subject.mesh Insulin, metabolism en_US
dc.subject.mesh Leptin, administration & dosage, metabolism en_US
dc.subject.mesh Animals en_US
dc.subject.mesh Motor Activity, physiology en_US
dc.subject.mesh Obesity, genetics, metabolism en_US
dc.subject.mesh Research Support, U.S. Gov't, P.H.S. en_US
dc.subject.mesh Phenotype en_US
dc.subject.mesh Research Support, Non-U.S. Gov't en_US
dc.subject.mesh Research Support, U.S. Gov't, Non-P.H.S. en_US
dc.subject.mesh Male en_US
dc.title Obesity and endocrine dysfunction in mice with deletions of both neuropeptide Y and galanin en_US
dc.type Article en_US

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