dc.contributorUniversidade Estadual Paulista (Unesp)
dc.date.accessioned2014-05-27T11:29:52Z
dc.date.accessioned2022-10-05T18:53:53Z
dc.date.available2014-05-27T11:29:52Z
dc.date.available2022-10-05T18:53:53Z
dc.date.created2014-05-27T11:29:52Z
dc.date.issued2013-07-01
dc.identifierCirculation. Heart failure, v. 6, n. 4, p. 809-816, 2013.
dc.identifier1941-3297
dc.identifierhttp://hdl.handle.net/11449/75826
dc.identifier10.1161/CIRCHEARTFAILURE.112.000298
dc.identifierWOS:000335157800031
dc.identifier2-s2.0-84884720901
dc.identifier3278528112652257
dc.identifier1213140801402647
dc.identifier0000-0002-5843-6232
dc.identifier0000-0002-2180-1814
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/3924749
dc.description.abstractThis study was aimed to evaluate the influence of vitamin D (VD) deficiency on cardiac metabolism, morphology, and function. Thus, we investigated the relationship of these changes with the length of the nutrient restriction. Male weanling Wistar rats were allocated into 4 groups: C2 (n=24), animals were fed an AIN-93G diet with 1000 IU VD/kg of chow and were kept under fluorescent light for 2 months; D2 (n=22), animals were fed a VD-deficient AIN-93G diet and were kept under incandescent light for 2 months; C4 (n=21) animals were kept in the same conditions of C2 for 4 months; and D4 (n=23) animals were kept in the same conditions of D2 for 4 months. Biochemical analyses showed lower β-hydroxyacyl coenzyme-A dehydrogenase activity and higher lactate dehydrogenase activity in VD-deficient animals. Furthermore, VD deficiency was related to increased cytokines release, oxidative stress, apoptosis, and fibrosis. Echocardiographic data showed left ventricular hypertrophy and lower fractional shortening and ejection fraction in VD-deficient animals. Difference became evident in the lactate dehydrogenase activity, left ventricular weight, right ventricle weight, and left ventricular mass after 4 months of VD deficiency. Our data indicate that VD deficiency is associated with energetic metabolic changes, cardiac inflammation, oxidative stress, fibrosis and apoptosis, cardiac hypertrophy, left chambers alterations, and systolic dysfunction. Furthermore, length of the restriction influenced these cardiac changes.
dc.languageeng
dc.relationCirculation. Heart failure
dc.relation4,200
dc.rightsAcesso restrito
dc.sourceScopus
dc.subjectcaspase 3
dc.subjectconnexin 43
dc.subjectconnexin 43 protein, rat
dc.subjectlactate dehydrogenase
dc.subjectanimal
dc.subjectcardiac remodeling
dc.subjectdisease model
dc.subjectechography
dc.subjectheart left ventricle hypertrophy
dc.subjectheart ventricle
dc.subjectheart ventricle remodeling
dc.subjectmale
dc.subjectmetabolism
dc.subjectorgan size
dc.subjectoxidative stress
dc.subjectpathology
dc.subjectpathophysiology
dc.subjectphysiology
dc.subjectrat
dc.subjecttime
dc.subjectvitamin D deficiency
dc.subjectAnimals
dc.subjectCaspase 3
dc.subjectConnexin 43
dc.subjectDisease Models, Animal
dc.subjectHeart Ventricles
dc.subjectHypertrophy, Left Ventricular
dc.subjectL-Lactate Dehydrogenase
dc.subjectMale
dc.subjectOrgan Size
dc.subjectOxidative Stress
dc.subjectRats
dc.subjectTime Factors
dc.subjectVentricular Remodeling
dc.subjectVitamin D Deficiency
dc.titleImpact of the length of vitamin D deficiency on cardiac remodeling.
dc.typeArtigo


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