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http://purl.uniprot.org/citations/9771748http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/9771748http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/9771748http://www.w3.org/2000/01/rdf-schema#comment"Brain serotonin and leptin signaling contribute substantially to the regulation of feeding and energy expenditure. Here we show that young adult mice with a targeted mutation of the serotonin 5-HT2C receptor gene consume more food despite normal responses to exogenous leptin administration. Chronic hyperphagia leads to a 'middle-aged'-onset obesity associated with a partial leptin resistance of late onset. In addition, older mice develop insulin resistance and impaired glucose tolerance. Mutant mice also responded more to high-fat feeding, leading to hyperglycemia without hyperlipidemia. These findings demonstrate a dissociation of serotonin and leptin signaling in the regulation of feeding and indicate that a perturbation of brain serotonin systems can predispose to type 2 diabetes."xsd:string
http://purl.uniprot.org/citations/9771748http://purl.org/dc/terms/identifier"doi:10.1038/2647"xsd:string
http://purl.uniprot.org/citations/9771748http://purl.org/dc/terms/identifier"doi:10.1038/2647"xsd:string
http://purl.uniprot.org/citations/9771748http://purl.uniprot.org/core/author"Dallman M.F."xsd:string
http://purl.uniprot.org/citations/9771748http://purl.uniprot.org/core/author"Dallman M.F."xsd:string
http://purl.uniprot.org/citations/9771748http://purl.uniprot.org/core/author"Nonogaki K."xsd:string
http://purl.uniprot.org/citations/9771748http://purl.uniprot.org/core/author"Nonogaki K."xsd:string
http://purl.uniprot.org/citations/9771748http://purl.uniprot.org/core/author"Strack A.M."xsd:string
http://purl.uniprot.org/citations/9771748http://purl.uniprot.org/core/author"Strack A.M."xsd:string
http://purl.uniprot.org/citations/9771748http://purl.uniprot.org/core/author"Tecott L.H."xsd:string
http://purl.uniprot.org/citations/9771748http://purl.uniprot.org/core/author"Tecott L.H."xsd:string
http://purl.uniprot.org/citations/9771748http://purl.uniprot.org/core/date"1998"xsd:gYear
http://purl.uniprot.org/citations/9771748http://purl.uniprot.org/core/date"1998"xsd:gYear
http://purl.uniprot.org/citations/9771748http://purl.uniprot.org/core/name"Nat. Med."xsd:string
http://purl.uniprot.org/citations/9771748http://purl.uniprot.org/core/name"Nat. Med."xsd:string
http://purl.uniprot.org/citations/9771748http://purl.uniprot.org/core/pages"1152-1156"xsd:string
http://purl.uniprot.org/citations/9771748http://purl.uniprot.org/core/pages"1152-1156"xsd:string
http://purl.uniprot.org/citations/9771748http://purl.uniprot.org/core/title"Leptin-independent hyperphagia and type 2 diabetes in mice with a mutated serotonin 5-HT2C receptor gene."xsd:string
http://purl.uniprot.org/citations/9771748http://purl.uniprot.org/core/title"Leptin-independent hyperphagia and type 2 diabetes in mice with a mutated serotonin 5-HT2C receptor gene."xsd:string
http://purl.uniprot.org/citations/9771748http://purl.uniprot.org/core/volume"4"xsd:string
http://purl.uniprot.org/citations/9771748http://purl.uniprot.org/core/volume"4"xsd:string
http://purl.uniprot.org/citations/9771748http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/9771748
http://purl.uniprot.org/citations/9771748http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/9771748