Please use this identifier to cite or link to this item: https://repositorio.uca.edu.ar/handle/123456789/1638
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dc.contributor.authorJiménez Ortega, Vanesaes
dc.contributor.authorRíos Lugo, María J.es
dc.contributor.authorCano Barquilla, Pilares
dc.contributor.authorCardinali, Daniel Pedroes
dc.contributor.authorEsquifino, Ana I.es
dc.contributor.authorFernández Mateos, Pilares
dc.contributor.authorSpinedi, Eduardo J.es
dc.date.accessioned2019-05-02T14:01:13Z-
dc.date.available2019-05-02T14:01:13Z-
dc.date.issued2015-
dc.identifier.citationRíos Lugo, M. J., et al. Melatonin counteracts changes in hypothalamic gene expression of signals regulating feeding behavior in high-fat fed rats [en línea]. Preprint del artículo publicado en Hormone Molecular Biology and Clinical Investigation. 2015, 21 (3). doi:10.1515/hmbci-2014-0041. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/1638es
dc.identifier.issn1868-1883 (impreso)-
dc.identifier.issn1868-1891 (online)-
dc.identifier.urihttps://repositorio.uca.edu.ar/handle/123456789/1638-
dc.description.abstractAbstract: Background: Previous studies indicate that the administration of melatonin caused body weight and abdominal visceral fat reductions in rodent models of hyperadiposity. The objective of the present study performed in high-fat fed rats was to evaluate the activity of melatonin on gene expression of some medial basal hypothalamus (MBH) signals involved in feeding behavior regulation, including neuropeptide Y (NPY), proopiomelanocortin (POMC), prolactin-releasing peptide (PrRP), leptin- and insulinreceptors (R) and insulin-R substrate (IRS)-1 and -2. Blood levels of leptin and adiponectin were also measured. Methods: Adult Wistar male rats were divided into four groups (n= 16/group): (i) control diet (3 % fat); (ii) high-fat (35 %) diet; (iii) high-fat diet + melatonin; (iv) control diet + melatonin. Rats had free access to high-fat or control chow and one of the following drinking solutions: (a) tap water; (b) 25 μg/mL of melatonin. Results: After 10 weeks, the high-fat fed rats showed augmented MBH mRNA levels of NPY, leptin-R, PrRP, insulin-R, IRS-1 and IRS-2. The concomitant administration of melatonin counteracted this increase. Feeding of rats with a high-fat diet augmented expression of MBH POMC gene through an effect insensitive to melatonin treatment. The augmented levels of circulating leptin and adiponectin seen in high-fat fed rats were counteracted by melatonin as was the augmented body weight: melatonin significantly attenuated body weight increase in high-fat fed rats without affecting chow or water consumption. Melatonin augmented plasma leptin and adiponectin in control rats. Conclusions: The results indicate that an effect on gene expression of feeding behavior signals at the CNS may complement a peripheral rise of the energy expenditure produced by melatonin to decrease body weight in high-fat fed ratses
dc.formatapplication/pdfes
dc.languageenges
dc.language.isoenges
dc.publisherDe Gruyteres
dc.rightsAcceso Abiertoes
dc.rights.urihttps://creativecommons.org/licenses/by-nc-sa/4.0/es
dc.sourcePreprint del artículo publicado en Hormone Molecular Biology and Clinical Investigation, Vol. 21, N° 3, 2015es
dc.subjectMELATONINAes
dc.subjectGRASAS EN LA DIETAes
dc.subjectALIMENTACIONes
dc.subjectEXPRESION GENICAes
dc.subjectNEUROPEPTIDO Yes
dc.subjectPROOPIOMELANOCORTINAes
dc.subjectPROLACTINAes
dc.subjectLEPTINAes
dc.subjectADIPONECTINAes
dc.subjectHIPOTALAMO MEDIOes
dc.titleMelatonin counteracts changes in hypothalamic gene expression of signals regulating feeding behavior in high-fat fed ratses
dc.typeArtículoes
dc.identifier.doi10.1515/hmbci-2014-0041-
uca.pathFacultad de Ciencias Médicas|Departamento de Docencia e Investigaciónes
uca.disciplinaMEDICINAes
uca.filename/home/data-uca-generic/folder_generic/IIBiomedicas/melatonin-counteracts-hypothalamic/metadata.xmles
uca.issnrd1es
uca.affiliationFil: Jiménez Ortega, Vanesa. Universidad Complutense. Facultad de Medicina. Departamento de Bioquímica y Biología Molecular III; Españaes
uca.affiliationFil: Ríos Lugo, María J. Universidad Complutense. Facultad de Medicina. Departamento de Bioquímica y Biología Molecular III; Españaes
uca.affiliationFil: Cano Barquilla, Pilar. Universidad Complutense. Facultad de Medicina. Departamento de Bioquímica y Biología Molecular III; Españaes
uca.affiliationFil: Cardinali, Daniel P. Pontificia Universidad Católica Argentina. Facultad de Ciencias Médicas. Instiuto de Investigaciones Biomédicas; Argentinaes
uca.affiliationFil: Cardinali, Daniel P. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes
uca.affiliationFil: Esquifino, Ana I. Universidad Complutense. Facultad de Medicina. Departamento de Bioquímica y Biología Molecular III; Españaes
uca.affiliationFil: Fernández Mateos, Pilar. Universidad Complutense. Facultad de Medicina. Departamento de Biología Celular; Españaes
uca.affiliationFil: Spinedi, Eduardo J. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentinaes
uca.affiliationFil: Spinedi, Eduardo J. Universidad Nacional de La Plata. Centro de Endocrinología Experimental y Aplicada; Argentinaes
uca.versionsubmittedVersiones
item.languageiso639-1en-
item.grantfulltextopen-
item.fulltextWith Fulltext-
crisitem.author.deptConsejo Nacional de Investigaciones Científicas y Técnicas-
crisitem.author.deptInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.orcid0000-0002-0813-9088-
crisitem.author.parentorgFacultad de Ciencias Médicas-
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