The finding of increased anti-inflammatory property by 1,25(OH)<sub>2</sub> D<sub>3</sub> through promotion of VDR and miR-126-3p expression in ECs provide plausible evidence that vitamin D deficiency and downregulation of VDR expression could contribute to increased inflammatory phenotypic changes in maternal vasculature in preeclampsia.
It focuses on several aspects related to cellular and molecular physiology such as VDR as the trigger point of vitamin D action, oxidative stress as a consequence of vitamin D deficiency.
Our findings for the first time indicated that there is a strong association between vitamin D deficiency, lipid profile and the VDR rs1544410G>A and rs7T41>G VDBP genes polymorphisms.
The gene expressions of vitamin D receptor and CYP27B1 and 25 hydroxyvitamin D plasma level ensured that the diets caused vitamin D deficiency or supplementation.
The exact association between Vitamin D deficiency and chronic disease conditions remains unclear; however, studies have focused on the mechanism of Vitamin D regulation by assessing the role of the Vitamin D associated genes/proteins such as VDR (Vitamin D receptor), VDBP (Vitamin D Binding protein), CYP27B1 as these are integral parts of the Vitamin D signaling pathway.
In addition, combined analysis of vitamin D levels and VDR mutants revealed association of vitamin D deficiencies and VDR mutants with chronic heart failure.
In addition, many preclinical studies in animals with vitamin D deficiency or genetically silenced expression of the vitamin D receptor or vitamin D metabolizing enzymes suggest that the absence of vitamin D action may result in cardiovascular events.
Serum vitamin D deficiency and vitamin D receptor gene polymorphism are associated with increased risk of cardiovascular disease in a Chinese rural population.
In patients with thrombotic state and vitamin D deficiency, vitamin D analogs and vitamin D receptor activators have been determined as adjunctive anticoagulant treatment in previous studies.
Recent evidence suggests vitamin D has a critical role in maintaining heart health through activation of the vitamin D receptor expressed in cardiomyocytes, and vitamin D deficiency may be implicated in the pathophysiology of HFrEF through activation of the renin-angiotensin system, impaired calcium handling, exaggerated inflammation, secondary hyperparathyroidism, pro-fibrotic properties, and proatherogenic potential.
Association between Vitamin D Deficiency and Single Nucleotide Polymorphisms in the Vitamin D Receptor and GC Genes and Analysis of Their Distribution in Mexican Postmenopausal Women.
Many, if not most cells have the hydroxylases necessary for intra-cellular activation of vitamin D. It is likely that more vitamin D diffuses or are transported into the cells than 25(OH)D and 1,25(OH)<sub>2</sub>D, and accordingly, most of the 1,25(OH)<sub>2</sub>D that bind to the VDR are derived from intra-cellular hydroxylation of vitamin D. Therefore, our hypothesis is that serum vitamin D is a better marker of a subject's vitamin D status than 25(OH)D. Since the half-life in serum for vitamin D is approximately one day, giving vitamin D weekly or monthly will result in short-lived serum vitamin D peaks with periods of vitamin D deficiency in between.
This study aims to investigate the association of vitamin D deficiency and vitamin D receptor (VDR) gene polymorphisms with susceptibility and severity to multidrug-resistant tuberculosis (MDR-TB) in comparison with drug-sensitive tuberculosis (DS-TB) and health controls in China.A total of 180 patients with pulmonary TB (128 DS-TB, 52 MDR-TB) and 59 healthy controls were enrolled into 3 groups.
Maternal vitamin D deficiency during pregnancy affects expression of adipogenic-regulating genes peroxisome proliferator-activated receptor gamma (PPARγ) and vitamin D receptor (VDR) in lean male mice offspring.
The purpose of this paper is to report the study design of a prospective eight week prospective double-blind randomized, placebo-controlled trial (n = 330 allocated 2:1 to intervention vs. control) to assess the effect of placebo vs. high-dose oral cholecalciferol (100,000 IU vitamin D3 at baseline and week 2) on 6-week change of select biologic cardiometabolic risk factors (including parathyroid hormone to assess biologic activity, pro-inflammatory/pro-thrombotic/fibrotic markers, insulin sensitivity and vitamin D metabolites) and their relationship to vitamin D administration and modification by vitamin D receptor polymorphisms in overweight, hypertensive African Americans with hypovitaminosis D. Findings from this trial will present insights into potential causal links between vitamin D repletion and mechanistic pathways of CV disease, including established and novel genomic markers.
However VDR gene polymorphisms did not seem to be associated with an increased risk of MS. <b>Conclusions:</b> Vitamin D deficiency, rs7975232, and rs1544410VDR gene variants are associated with MS parameters in Russian middle-aged women.
Here, we sought to study the impact of the vitamin D receptor (Vdr) on adipocyte size in young and old mice and the effect of maternal vitamin D deficiency on fetal adipogenesis.
The aim of the study was to evaluate markers of oxidative stress and vitamin D receptor in paraspinal muscles in low back pain patients with vitamin D deficiency, with normal level of vitamin D, and after 5 weeks of vitamin D supplementation.