Mostrar el registro sencillo del ítem
dc.contributor.author
Cravo, Roberta M.
dc.contributor.author
Frazao, Renata
dc.contributor.author
Perello, Mario
dc.contributor.author
Osborne-Lawrence, Sherri
dc.contributor.author
Williams, Kevin W
dc.contributor.author
Zigman, Jeffery M.
dc.contributor.author
Vianna, Claudia
dc.contributor.author
Elias, Carol F.
dc.date.available
2015-05-27T16:45:16Z
dc.date.issued
2013-03-07
dc.identifier.citation
Cravo, Roberta M.; Frazao, Renata; Perello, Mario; Osborne-Lawrence, Sherri; Williams, Kevin W; Zigman, Jeffery M.; Vianna, Claudia; Elias, Carol F.; Leptin signaling in Kiss1 neurons arises after pubertal development; Public Library Science; Plos One; 7-3-2013; 58698-58699;
dc.identifier.issn
1932-6203
dc.identifier.uri
http://hdl.handle.net/11336/580
dc.description.abstract
The adipocyte-derived hormone leptin is required for normal pubertal maturation in mice and humans and, therefore, leptin has been recognized as a crucial metabolic cue linking energy stores and the onset of puberty. Several lines of evidence have suggested that leptin acts via kisspeptin expressing neurons of the arcuate nucleus to exert its effects. Using conditional knockout mice, we have previously demonstrated that deletion of leptin receptors (LepR) from kisspeptin cells cause no puberty or fertility deficits. However, developmental adaptations and system redundancies may have obscured the physiologic relevance of direct leptin signaling in kisspeptin neurons. To overcome these putative effects, we re-expressed endogenous LepR selectively in kisspeptin cells of mice otherwise null for LepR, using the Cre-loxP system. Kiss1-Cre LepR null mice showed no pubertal development and no improvement of the metabolic phenotype, remaining obese, diabetic and infertile. These mice displayed decreased numbers of neurons expressing Kiss1 gene, similar to prepubertal control mice, and an unexpected lack of re-expression of functional LepR. To further assess the temporal coexpression of Kiss1 and Lepr genes, we generated mice with the human renilla green fluorescent protein (hrGFP) driven by Kiss1 regulatory elements and crossed them with mice that express Cre recombinase from the Lepr locus and the R26-tdTomato reporter gene. No coexpression of Kiss1 and LepR was observed in prepubertal mice. Our findings unequivocally demonstrate that kisspeptin neurons are not the direct target of leptin in the onset of puberty. Leptin signaling in kisspeptin neurons arises only after completion of sexual maturation.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Public Library Science
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Hipotalamo
dc.subject
Neuropeptidos
dc.subject
Leptina
dc.subject.classification
Ciencias Médicas y de la Salud
dc.subject.classification
Medicina Básica
dc.subject.classification
Neurociencias (incluye Psicofiosiología)
dc.title
Leptin signaling in Kiss1 neurons arises after pubertal development
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2016-03-30 10:35:44.97925-03
dc.journal.pagination
58698-58699
dc.journal.pais
Estados Unidos
dc.journal.ciudad
San Francisco
dc.description.fil
Fil: Cravo, Roberta M..
dc.description.fil
Fil: Frazao, Renata.
dc.description.fil
Fil: Perello, Mario. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Cs.fisiologicas. Laboratorio de Neurofisiologia;
dc.description.fil
Fil: Osborne-Lawrence, Sherri.
dc.description.fil
Fil: Williams, Kevin W.
dc.description.fil
Fil: Zigman, Jeffery M..
dc.description.fil
Fil: Vianna, Claudia.
dc.description.fil
Fil: Elias, Carol F..
dc.journal.title
Plos One
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.1371/journal.pone.0058698
Archivos asociados