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dc.contributor.author
Alsina, Ramiro
dc.contributor.author
Trotta, Milagros
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dc.contributor.author
Bumaschny, Viviana Florencia
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dc.date.available
2019-10-31T20:04:06Z
dc.date.issued
2018-09
dc.identifier.citation
Alsina, Ramiro; Trotta, Milagros; Bumaschny, Viviana Florencia; Hypothalamic Proopiomelanocortin Is Necessary for Normal Glucose Homeostasis in Female Mice; Frontiers Research Foundation; Frontiers in Endocrinology; 9; 554; 9-2018; 1-7
dc.identifier.issn
1664-2392
dc.identifier.uri
http://hdl.handle.net/11336/87781
dc.description.abstract
The arcuate nucleus of the hypothalamus is a key regulator of energy balance and glucose homeostasis. In particular, arcuate proopiomelanocortin (POMC) neurons inhibit food intake, stimulate energy expenditure and increase glucose tolerance. The interruption of insulin or glucose signaling in POMC neurons leads to glucose intolerance without changing energy homeostasis. Although it was previously shown that POMC neurons are necessary for normal glucose homeostasis, the participation of POMC neuropeptide, by mechanisms independent of energy balance, remains to be demonstrated. To study the role of POMC in the regulation of glucose homeostasis, we performed glucose and insulin tolerance tests in non-obese mice lacking hypothalamic POMC expression. We found that POMC deficiency leads to glucose intolerance and insulin resistance in female mice before the onset of obesity or hyperphagia. Conversely, POMC deficiency does not impair glucose homeostasis in non-obese male mice. Interestingly, females completely normalize both glucose and insulin tolerance after genetic POMC restoration. Next, to further study sex dimorphism of POMC neurons regarding glucose homeostasis, we measured glucose-elicited changes in C-FOS by performing immunofluorescence in brain slices of POMC-EGFP mice. Remarkably, we found that glucose-induced C-FOS expression in POMC neurons is more than 3-fold higher in female than in male mice. Altogether, our results reveal a key role of arcuate POMC in the regulation of glucose homeostasis in females. Since POMC reactivation completely reverses the diabetogenic phenotype, arcuate POMC could be a potential target for diabetes therapy.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Frontiers Research Foundation
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dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by/2.5/ar/
dc.subject
DIABETES
dc.subject
ESR1
dc.subject
GLUCOSE TOLERANCE
dc.subject
HYPOTHALAMUS
dc.subject
INSULIN SENSITIVITY
dc.subject
PROOPIOMELANOCORTIN
dc.subject.classification
Fisiología
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dc.subject.classification
Medicina Básica
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dc.subject.classification
CIENCIAS MÉDICAS Y DE LA SALUD
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dc.title
Hypothalamic Proopiomelanocortin Is Necessary for Normal Glucose Homeostasis in Female 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
2019-10-16T18:52:28Z
dc.journal.volume
9
dc.journal.number
554
dc.journal.pagination
1-7
dc.journal.pais
Suiza
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dc.description.fil
Fil: Alsina, Ramiro. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
dc.description.fil
Fil: Trotta, Milagros. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina
dc.description.fil
Fil: Bumaschny, Viviana Florencia. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Ciencias Fisiológicas; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina
dc.journal.title
Frontiers in Endocrinology
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://www.frontiersin.org/articles/10.3389/fendo.2018.00554/full
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/http://dx.doi.org/10.3389/fendo.2018.00554
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