RDF/XMLNTriplesTurtleShow queryShare
SubjectPredicateObject
http://purl.uniprot.org/citations/20923696http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/20923696http://www.w3.org/2000/01/rdf-schema#comment"Obesity is associated with increased risk of diabetes, cardiovascular disease and several types of cancers. The hypothalamus is a region of the brain critical in the regulation of body weight. One of the critical and best studied hypothalamic circuits is comprised of the melanocortinergic orexigenic agouti-related protein (AgRP) and anorexigenic α-melanocyte stimulating hormone (α-MSH) neurons. These neurons project axons to the same hypothalamic target neurons and balance each other's activity leading to body weight regulation. We previously showed that the brain proteoglycan syndecan-3 regulates feeding behavior and body weight, and syndecan-3 null (SDC-3(-/-)) mice are lean and obesity resistant. Here we show that the melanocortin agonist Melanotan II (MTII) potently suppresses food intake and activates the hypothalamic paraventricular nuclei (PVN) in SDC-3(-/-) mice based on c-fos immunoreactivity. Interestingly, we determined that the AgRP neuropeptide is reduced in the PVN of SDC-3(-/-) mice compared to wild type mice. In contrast, neuropeptide Y, coexpressed in the AgRP neuron, is not differentially expressed nor is the counteracting neuropeptide α-MSH. These findings are unprecedented and indicate that AgRP protein localization can be selectively regulated within the hypothalamus resulting in altered neuropeptide response and tone."xsd:string
http://purl.uniprot.org/citations/20923696http://purl.org/dc/terms/identifier"doi:10.1016/j.neuroscience.2010.09.060"xsd:string
http://purl.uniprot.org/citations/20923696http://purl.uniprot.org/core/author"Zhu J."xsd:string
http://purl.uniprot.org/citations/20923696http://purl.uniprot.org/core/author"Zheng Q."xsd:string
http://purl.uniprot.org/citations/20923696http://purl.uniprot.org/core/author"Horvath T.L."xsd:string
http://purl.uniprot.org/citations/20923696http://purl.uniprot.org/core/author"Reizes O."xsd:string
http://purl.uniprot.org/citations/20923696http://purl.uniprot.org/core/author"Clegg D.J."xsd:string
http://purl.uniprot.org/citations/20923696http://purl.uniprot.org/core/author"Borok E."xsd:string
http://purl.uniprot.org/citations/20923696http://purl.uniprot.org/core/author"Benoit S.C."xsd:string
http://purl.uniprot.org/citations/20923696http://purl.uniprot.org/core/author"Shanabrough M."xsd:string
http://purl.uniprot.org/citations/20923696http://purl.uniprot.org/core/date"2010"xsd:gYear
http://purl.uniprot.org/citations/20923696http://purl.uniprot.org/core/name"Neuroscience"xsd:string
http://purl.uniprot.org/citations/20923696http://purl.uniprot.org/core/pages"1032-1040"xsd:string
http://purl.uniprot.org/citations/20923696http://purl.uniprot.org/core/title"Enhanced anorexigenic signaling in lean obesity resistant syndecan-3 null mice."xsd:string
http://purl.uniprot.org/citations/20923696http://purl.uniprot.org/core/volume"171"xsd:string
http://purl.uniprot.org/citations/20923696http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/20923696
http://purl.uniprot.org/citations/20923696http://xmlns.com/foaf/0.1/primaryTopicOfhttps://pubmed.ncbi.nlm.nih.gov/20923696
http://purl.uniprot.org/uniprot/#_B1ASF6-mappedCitation-20923696http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20923696
http://purl.uniprot.org/uniprot/#_Q64519-mappedCitation-20923696http://www.w3.org/1999/02/22-rdf-syntax-ns#objecthttp://purl.uniprot.org/citations/20923696
http://purl.uniprot.org/uniprot/Q64519http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/20923696
http://purl.uniprot.org/uniprot/B1ASF6http://purl.uniprot.org/core/mappedCitationhttp://purl.uniprot.org/citations/20923696