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(Reference retrieved automatically from Web of Science through information on FAPESP grant and its corresponding number as mentioned in the publication by the authors.)

Impact of the Length of Vitamin D Deficiency on Cardiac Remodeling

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Assalin, Heloisa Balan [1] ; Rafacho, Bruna Paola [1] ; dos Santos, Priscila Portugal [1] ; Ardisson, Lidiane Paula [1] ; Roscani, Meliza Goi [1] ; Chiuso-Minicucci, Fernanda [2] ; Barbisan, Luis Fernando [3] ; Henrique Fernandes, Ana Angelica [4] ; Azevedo, Paula Schmidt [1] ; Minicucci, Marcos Ferreira [1] ; Zornoff, Leonardo Antonio [1] ; Rupp de Paiva, Sergio Alberto [1]
Total Authors: 12
Affiliation:
[1] Sao Paulo State Univ, Dept Internal Med, Botucatu Med Sch, UNESP, Inst Biosci, BR-18618000 Botucatu, SP - Brazil
[2] Sao Paulo State Univ, Dept Microbiol & Immunol, UNESP, Inst Biosci, BR-18618000 Botucatu, SP - Brazil
[3] Sao Paulo State Univ, Dept Morphol, UNESP, Inst Biosci, BR-18618000 Botucatu, SP - Brazil
[4] Sao Paulo State Univ, Dept Chem & Biochem, UNESP, Inst Biosci, BR-18618000 Botucatu, SP - Brazil
Total Affiliations: 4
Document type: Journal article
Source: Circulation-Heart Failure; v. 6, n. 4, p. 809-816, JUL 2013.
Web of Science Citations: 35
Abstract

Background This 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. Methods and Results 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 -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. Conclusions 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. (AU)