Please use this identifier to cite or link to this item: https://repositorio.uca.edu.ar/handle/123456789/1657
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dc.contributor.authorCano Barquilla, Pilares
dc.contributor.authorPagano, Eleonora Samantaes
dc.contributor.authorJiménez Ortega, Vanesaes
dc.contributor.authorFernández Mateos, Pilares
dc.contributor.authorEsquifino, Ana I.es
dc.contributor.authorCardinali, Daniel Pedroes
dc.date.accessioned2019-05-02T14:01:18Z-
dc.date.available2019-05-02T14:01:18Z-
dc.date.issued2014-
dc.identifier.citationCano Barquilla, P., et al. Melatonin normalizes clinical and biochemical parameters of mild inflammation in diet-induced metabolic syndrome in rats [en línea]. Preprint del documento publicado en Journal of Pineal Research 2014, 57. doi:10.1111/jpi.12168. Disponible en: https://repositorio.uca.edu.ar/handle/123456789/1657es
dc.identifier.issn0742-3098 (impreso)-
dc.identifier.issn1600-079X (online)-
dc.identifier.urihttps://repositorio.uca.edu.ar/handle/123456789/1657-
dc.description.abstractAbstract: The objective of the present study was to evaluate the efficacy of melatonin to affect mild inflammation in the metabolic syndrome (MS) induced by a high-fat diet in rats. 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) melatonin. Rats had free access to high-fat or control chow and one of the following drinking solutions for 10 weeks: (a) tap water; (b) 25 μg/mL of melatonin. Plasma interleukin (IL)-1β, IL-4, IL-6, IL-10, tumor necrosis factor (TNF)-α, interferon (IFN)-γ and C-reactive protein (CRP) were measured at two time intervals, i.e. the middle of daylight period and the middle of the scotophase. In addition, a number of somatic and metabolic components employed clinically to monitor the MS were measured. Melatonin decreased the augmented circulating levels of IL-1β, IL-6, TNF-α, IFN-γ and CRP seen in obese rats and restored the depressed levels of IL-4 and IL-10. Rats fed with the high-fat diet showed significantly higher body weights and augmented systolic blood pressure from the 3rd and 4th week onwards, respectively, melatonin effectively preventing these changes. In high-fat fed rats circulating low-density lipoprotein-cholesterol, total cholesterol and triglyceride concentration augmented significantly, melatonin being effective to counteract these changes. Melatonin-treated rats showed a decreased insulin resistance, the highest values of plasma high-density lipoprotein-cholesterol and the lowest values of plasma uric acid. The results indicate that melatonin is able to normalize the altered biochemical proinflammatory profile seen in rats fed with a high-fat dietes
dc.formatapplication/pdfes
dc.languageenges
dc.language.isoenges
dc.rightsAcceso Abiertoes
dc.rights.urihttps://creativecommons.org/licenses/by-nc-sa/4.0/es
dc.sourcePreprint del documento publicado en Journal of pineal research, Nº 57, 2014es
dc.subjectDISLIPIDEMIAes
dc.subjectTOLERANCIA A LA GLUCOSAes
dc.subjectDIETAes
dc.subjectHIPERTENSIONes
dc.subjectINFLAMACIONes
dc.subjectACIDO URICOes
dc.titleMelatonin normalizes clinical and biochemical parameters of mild inflammation in diet-induced metabolic syndrome in ratses
dc.typeArtículoes
dc.identifier.doi10.1111/jpi.12168-
uca.pathFacultad de Ciencias Médicas|Departamento de Docencia e Investigaciónes
uca.disciplinaMEDICINAes
uca.filename/home/data-uca-generic/folder_generic/IIBiomedicas/melatonin-normalizes-clinical-biochemical/metadata.xmles
uca.issnrd1es
uca.affiliationFil: Cano Barquilla, Pilar. Universidad Complutense. Facultad de Medicina. Departamento de Bioquímica y Biología Molecular III; Españaes
uca.affiliationFil: Pagano, Eleonora S. Pontifica Universidad Católica Argentina. Faculta de Ciencias Médicas. Departamento de Docencia e Investigación; Argentinaes
uca.affiliationFil: Jiménez Ortega, Vanesa. 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: Esquifino, Ana I. Universidad Complutense. Facultad de Medicina. Departamento de Bioquímica y Biología Molecular III; Españaes
uca.affiliationFil: Cardinali, Daniel P. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Fisiología; Argentinaes
uca.versionsubmittedVersiones
item.languageiso639-1en-
item.grantfulltextopen-
item.fulltextWith Fulltext-
crisitem.author.deptInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.deptLaboratorio de Psiconeuroendocrinoinmunología-
crisitem.author.deptConsejo Nacional de Investigaciones Científicas y Técnicas-
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-
crisitem.author.parentorgInstituto de Investigaciones Biomédicas - BIOMED-
crisitem.author.parentorgFacultad de Ciencias Médicas-
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