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dc.contributor.author
Fernandez, Gimena  
dc.contributor.author
Cabral, Agustina Soledad  
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Andreoli, Maria Florencia  
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Labarthe, Alexandra  
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M'Kadmi, Céline  
dc.contributor.author
Ramos, Jorge Guillermo  
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Marie, Jacky  
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Fehrentz, Jean-Alain  
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Epelbaum, Jacques  
dc.contributor.author
Tolle, Virginie  
dc.contributor.author
Perello, Mario  
dc.date.available
2018-12-19T13:33:03Z  
dc.date.issued
2018-02  
dc.identifier.citation
Fernandez, Gimena; Cabral, Agustina Soledad; Andreoli, Maria Florencia; Labarthe, Alexandra; M'Kadmi, Céline; et al.; Evidence supporting a role for constitutive ghrelin receptor signaling in fasting-induced hyperphagia in male mice; Endocrine Society; Endocrinology; 159; 2; 2-2018; 1021-1034  
dc.identifier.issn
0013-7227  
dc.identifier.uri
http://hdl.handle.net/11336/66726  
dc.description.abstract
Ghrelin is a potent orexigenic peptide hormone that acts through the growth hormone secretagogue receptor (GHSR), a G protein–coupled receptor highly expressed in the hypothalamus. In vitro studies have shown that GHSR displays a high constitutive activity, whose physiological relevance is uncertain. As GHSR gene expression in the hypothalamus is known to increase in fasting conditions, we tested the hypothesis that constitutive GHSR activity at the hypothalamic level drives the fasting-induced hyperphagia. We found that refed wild-type (WT) mice displayed a robust hyperphagia that continued for 5 days after refeeding and changed their food intake daily pattern. Fasted WT mice showed an increase in plasma ghrelin levels, as well as in GHSR expression levels and ghrelin binding sites in the hypothalamic arcuate nucleus. When fasting-refeeding responses were evaluated in ghrelin- or GHSR-deficient mice, only the latter displayed an;15% smaller hyperphagia, compared with WT mice. Finally, fasting-induced hyperphagia of WT mice was significantly smaller in mice centrally treated with the GHSR inverse agonist K-(D-1-Nal)-FwLL-NH2, compared with mice treated with vehicle, whereas it was unaffected in mice centrally treated with the GHSR antagonists D-Lys3-growth hormone–releasing peptide 6 or JMV2959. Taken together, genetic models and pharmacological results support the notion that constitutive GHSR activity modulates the magnitude of the compensatory hyperphagia triggered by fasting. Thus, the hypothalamic GHSR signaling system could affect the set point of daily food intake, independently of plasma ghrelin levels, in situations of negative energy balance. (Endocrinology 159: 1021–1034, 2018)  
dc.format
application/pdf  
dc.language.iso
eng  
dc.publisher
Endocrine Society  
dc.rights
info:eu-repo/semantics/openAccess  
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/  
dc.subject
Ghrelin  
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Fasting  
dc.subject
Appetite  
dc.subject.classification
Inmunología  
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Medicina Básica  
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CIENCIAS MÉDICAS Y DE LA SALUD  
dc.title
Evidence supporting a role for constitutive ghrelin receptor signaling in fasting-induced hyperphagia in male mice  
dc.type
info:eu-repo/semantics/article  
dc.type
info:ar-repo/semantics/artículo  
dc.type
info:eu-repo/semantics/publishedVersion  
dc.date.updated
2018-10-22T21:51:02Z  
dc.journal.volume
159  
dc.journal.number
2  
dc.journal.pagination
1021-1034  
dc.journal.pais
Estados Unidos  
dc.description.fil
Fil: Fernandez, Gimena. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto Multidisciplinario de Biología Celular. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Instituto Multidisciplinario de Biología Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biología Celular; Argentina  
dc.description.fil
Fil: Cabral, Agustina Soledad. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto Multidisciplinario de Biología Celular. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Instituto Multidisciplinario de Biología Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biología Celular; Argentina  
dc.description.fil
Fil: Andreoli, Maria Florencia. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Universidad Nacional del Litoral; Argentina  
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Fil: Labarthe, Alexandra. Universite Paris Descartes; Francia  
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Fil: M'Kadmi, Céline. Centre National de la Recherche Scientifique; Francia  
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Fil: Ramos, Jorge Guillermo. Universidad Nacional del Litoral; Argentina  
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Fil: Marie, Jacky. Centre National de la Recherche Scientifique; Francia  
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Fil: Fehrentz, Jean-Alain. Centre National de la Recherche Scientifique; Francia  
dc.description.fil
Fil: Epelbaum, Jacques. Universite Paris Descartes; Francia. Museum National d'Histoire Naturelle; Francia  
dc.description.fil
Fil: Tolle, Virginie. Universite Paris Descartes; Francia  
dc.description.fil
Fil: Perello, Mario. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto Multidisciplinario de Biología Celular. Provincia de Buenos Aires. Gobernación. Comisión de Investigaciones Científicas. Instituto Multidisciplinario de Biología Celular. Universidad Nacional de La Plata. Instituto Multidisciplinario de Biología Celular; Argentina  
dc.journal.title
Endocrinology  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://dx.doi.org/10.1210/en.2017-03101  
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://academic.oup.com/endo/article-abstract/159/2/1021/4780800?redirectedFrom=fulltext