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Participation of fibroblast growth factor-23 (FGF -23) on oxidative stress, inflammatory mediators, energy metabolism, apoptosis and cardiac morphological and functional changes associated with vitamin D supplementation in rats


Vitamin D deficiency/insufficient has become public health problem. Additionally, it has encouraged the indiscriminate use of this vitamin. Vitamin D supplementation causes oxidative stress, inflammation, apoptosis, change energy metabolism and morphology and cardiac function. In addition, vitamin D supplementation increases serum phosphorus and hyperphosphatemia stimulates the release of fibroblast growth factor-23 (FGF-23). The increase of FGF-23 is associated with cardiac remodeling. The decrease in fosfatemia, by sevelamer hydrochloride, can attenuate the heart changes promoted by supplementation of vitamin D. Thus, the aim of this study is to verify that sevelamer hydrochloride treatment would decrease the concentration of FGF-23 and, consequently, would attenuate cardiac remodeling, resulting from vitamin D supplementation. The experiment will be used 80 Wistar male rats allocated into four groups: 1) Control group, fed standard chow (C, n=20); 2) Control group + 3% of sevelamer hydrochloride (S, n=20); 3) Vitamin D group supplemented with 10,000 IU of cholecalciferol/kg of chow (VD10, n=20); 4) Vitamin D group supplemented with 10,000 IU of cholecalciferol/kg of chow + 3% of sevelamer hydrochloride (VD10-S, n=20). After four months, animals will be undergoing echocardiography, euthanized and collecting biological material for carrying out the histological analysis, biochemical and molecular. (AU)

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