Age, serum 25-hydroxyvitamin D and vitamin D receptor (VDR) expression and function in peripheral blood mononuclear cells.
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ABSTRACT:
SUBMITTER: Coleman LA
PROVIDER: S-EPMC5094941 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:Low blood levels of the vitamin D metabolite 25-hydroxyvitamin D [25(OH)D] have been associated with an increased risk and poorer outcomes of various cancers, including hematological malignancies. The Central Kazakhstan area has a relatively high incidence rate of leukemia. However, the relationship between vitamin D status and leukemia or other types of cancer in Kazakhstan has not yet been addressed. Therefore, in this first pilot single-center study conducted in Central Kazakhstan, we compared plasma levels of 25(OH)D and the vitamin D receptor (VDR) gene expression levels in peripheral blood mononuclear cells of patients with leukemia and demographically matching healthy volunteers. The levels of 25(OH)D in patients were found to be significantly lower (10.8 ± 7.0 ng/mL; n = 31) than in healthy subjects (21.6 ± 7.8 ng/mL; n = 34; p < 0.0001). A similar difference was observed in both younger (<60 years old) and older (>60 years old) participants, though there was no association between 25(OH)D concentration and age within the patient group. In female patients, 25(OH)D levels were significantly lower than in male patients (p = 0.04). No significant seasonal variations of 25(OH)D were observed in either the patient or the control group. VDR gene expression levels appeared to be similar in leukemia patients and healthy subjects, and no correlation between the cellular VDR expression and plasma 25(OH)D concentrations was observed in either group of participants. We did not observe a significant association of 25(OH)D or VDR levels and overall survival of leukemia patients. This observational study conducted for the first time in Kazakhstan supports previous findings demonstrating reduced blood 25(OH)D levels in cancer (leukemia) patients. Larger studies are required to determine whether low 25(OH)D plasma concentrations represent a risk factor for leukemia development and/or progression.
| S-EPMC7281978 | biostudies-literature
Project description:A normal vitamin D status is essential for human health. Vitamin D deficiency is a recognized risk factor for all-cause mortality in normal individuals and in chronic kidney disease (CKD) patients. The link between vitamin D deficiency and death is a defective activation of the vitamin D receptor (VDR) by 1,25-dihydroxyvitamin D (calcitriol, the vitamin D hormone) to induce/repress genes that maintain mineral homeostasis and skeletal integrity, and prevent secondary hyperparathyroidism, hypertension, immune disorders, and renal and cardiovascular (CV) damage. The kidney is the main site for the conversion of 25-hydroxyvitamin D (25D) to circulating calcitriol, and therefore essential for the health benefits of endocrine VDR activation. The kidney is also essential for the uptake of 25D from the glomerular ultrafiltrate for its recycling to the circulation to maintain serum 25D levels, extrarenal calcitriol synthesis, and the prosurvival benefits of autocrine/paracrine VDR activation. Indeed, both calcitriol and vitamin D deficiency increase progressively in the course of CKD, and associate directly with accelerated disease progression and death. Therefore, the safe correction of calcitriol and vitamin D deficiency/insufficiency is becoming a high priority among nephrologists. This review updates the pathophysiology behind 25D and calcitriol deficiency and impaired VDR activation in CKD, the adequacy of current recommendations for vitamin D supplementation, and potential markers of the efficacy of therapy to prevent or slow the development of renal and CV lesions unrelated to parathyroid hormone suppression, a knowledge required for the design of trials to obtain evidence-based recommendations for vitamin D and calcitriol replacement at all stages of CKD.
| S-EPMC4089671 | biostudies-other
Project description:BackgroundAssociation of Vitamin D receptor (VDR) polymorphisms with lumbar disc herniation (LDH) have been identified in several ethnic groups globally. Despite abundant sunlight, vitamin D deficiency is reported in many tropical countries. As vitamin D is a key modulator for intestinal calcium absorption, low vitamin D could contribute to low serum calcium leading to abnormalities of skeletal homeostasis. Therefore, present study was aimed to study the association of serum 25-hydroxyvitamin D (25(OH)D), serum calcium and VDR polymorphisms in a selected Sri Lankan population.Materials & methodsA case control study was conducted in 119 participants (cases = 51: controls = 68). Serum 25(OH)D levels were measured using ELISA. The VDR polymorphisms (Fok I and Taq I) were detected by polymerase chain reaction followed by restriction fragment length polymorphism.ResultsFindings indicated a significantly low (p = 0.000) 25(OH)D levels in cases (18.7±3.7 ng/mL) compared to controls(25.5±9.8 ng/mL) while 25(OH)D in both groups were below the reference range. Mean serum calcium levels in both groups were within normal reference range and was not significantly different among groups. Statistically significant association was not observed between VDR Fok I polymorphisms among cases and controls. Although Fok I polymorphism genotypes were in Hardy-Weinberg equilibrium (HWE), Taq I genotypes in controls violated HWE.ConclusionPresent study confirms that insufficient serum 25(OH)D levels in cases have major contribution to LDH. VDR Fok I polymorphisms did not have any significant association with LDH in Sri Lankan ethnicity.
| S-EPMC6200232 | biostudies-literature
Project description:Climate change is expected to increase the frequency of extreme weather events, such as extended heat waves and droughts in the northern hemisphere. Besides affecting ecosystems worldwide, these changes in climate patterns will also affect the environmental health of human populations. While the medical community is mostly concerned with the negative impact of climate change, there might also be some beneficial effects. In this study we used laboratory data from a large university clinic in Germany (n = 13 406), to test for any detectable impact of two extreme summers on Vitamin-D [25(OH)D] plasma concentrations over a six year period (2014-2019). For the two years with extreme summers (2018 and 2019) the 25(OH)D plasma concentrations were significantly higher than in the previous four years (p < 0.001). A time series analysis (autoregressive term, AR, φ = 0.84, with an AR of one indicating a persistent effect) showed that 25(OH)D concentrations rise by 0.04 nmol/l (95% CI: 0.04-0.05 nmol/l) per hour of sunshine. The incidence of vitamin D deficiency was generally high (60% for 2014-2017) but dropped by 10% in 2018 and 2019. As such, the summers of 2018 and 2019, which are among the hottest and driest in Germany since the start of modern climate recordings, had a measurable positive effect on 25(OH)D plasma levels of the examined population. Given that 25(OH)D deficiency is widespread in higher latitudes, this implies that while mostly considered negative, climate change might also confer some health benefits with regard to vitamin D related medical conditions.
| S-EPMC7654803 | biostudies-literature
Project description:We have carried out melanoma case-control comparisons for six vitamin D receptor (VDR) gene single nucleotide polymorphisms (SNPs) and serum 25-hydroxyvitamin D(3) levels in order to investigate the role of vitamin D in melanoma susceptibility. There was no significant evidence of an association between any VDR SNP and risk in 1028 population-ascertained cases and 402 controls from Leeds, UK. In a second Leeds case-control study (299 cases and 560 controls) the FokI T allele was associated with increased melanoma risk (odds ratio (OR) 1.42, 95% confidence interval (CI) 1.06-1.91, p=0.02). In a meta-analysis in conjunction with published data from other smaller data sets (total 3769 cases and 3636 controls), the FokI T allele was associated with increased melanoma risk (OR 1.19, 95% CI 1.05-1.35), and the BsmI A allele was associated with a reduced risk (OR 0.81, 95% CI 0.72-0.92), in each instance under a parsimonious dominant model. In the first Leeds case-control comparison cases were more likely to have a higher body mass index (BMI) than controls (p=0.007 for linear trend). There was no evidence of a case-control difference in serum 25-hydroxyvitamin D(3) levels. In 1043 incident cases from the first Leeds case-control study, a single estimation of serum 25-hydroxyvitamin D(3) level taken at recruitment was inversely correlated with Breslow thickness (p=0.03 for linear trend). These data provide evidence to support the view that vitamin D and VDR may have a small but potentially important role in melanoma susceptibility, and putatively a greater role in disease progression.
| S-EPMC2786912 | biostudies-literature
Project description:ContextAdequate serum 25-hydroxyvitamin D concentrations, [25(OH)D], are required for optimal bone health, and low levels are associated with chronic diseases.ObjectiveWe investigated whether 41 candidate single nucleotide polymorphisms (SNPs) in vitamin D and calcium pathway genes (GC, DHCR7, CYP2R1, CYP27B1, CYP24A1, VDR, and CASR) are associated with [25(OH)D] or modify the increase in [25(OH)D] from vitamin D3 supplementation.Design and settingBaseline and year 1 [25(OH)D] measurements from a randomized controlled trial conducted at 11 clinical centers in the United States.ParticipantsA total of 1787 healthy non-Hispanic white participants aged 45-75 years.InterventionsVitamin D3 (1000 IU/d), calcium carbonate (1200 mg/d elemental), both, or placebo.Main outcome measuresGenotype main effects and interactions with vitamin D3 treatment estimated using multiple linear regression.ResultsThe baseline serum [25(OH)D] was 25.4 ± 8.7 ng/mL (mean ± SD). Associations with baseline levels were discovered for SNPs in CYP24A1 (rs2209314, rs2762939) and confirmed for SNPs in GC and CYP2R1. After 1 year, [25(OH)D] increased on average by 6.1 ± 8.9 ng/mL on vitamin D3 treatment and decreased by 1.1 ± 8.4 ng/mL on placebo. The increase in [25(OH)D] due to vitamin D3 supplementation was modified by genotypes at rs10766197 near CYP2R1, rs6013897 near CYP24A1, and rs7968585 near VDR.ConclusionsThe increase in [25(OH)D] attributable to vitamin D3 supplementation may vary according to common genetic differences in vitamin D 25-hydroxylase (CYP2R1), 24-hydroxylase (CYP24A1), and the vitamin D receptor (VDR) genes. These findings have implications for achieving optimal vitamin D status and potentially for vitamin D-related health outcomes.
| S-EPMC4184076 | biostudies-literature
Project description:Vitamin D is known to alter immune regulation. It binds to the vitamin D receptors (VDR) expressed on T lymphocytes and macrophages. In individuals with Hashimoto's thyroiditis, serum vitamin D levels were found to be lower compared to healthy controls. The study's objective was to investigate the association between VDR gene polymorphism (rs2228570) with blood serum levels of 25-OH vitamin D in patients with thyroid pathology from western Ukraine. The study involved a total of 153 patients with various forms of thyroid pathology. 25-OH vitamin D levels in the serum of the patients and healthy individuals were quantified with ELISA using the 25-OH vitamin D Total (Vit D-Direct) Test System ELISA Kit (Monobind Inc.®, United States, Product Code: 9425-300) on the EIA Reader Sirio S (Seac, Italy). Genotyping of the VDR (rs2228570) gene polymorphism was performed using TaqMan probes and TaqMan Genotyping Master Mix (4371355) on CFX96™Real-Time PCR Detection System (Bio-Rad Laboratories, Inc., USA). Polymerase chain reaction (PCR) for TaqMan genotyping was carried out according to the kit instructions (Applied Biosystems, USA). Our research identified that that genotype variants of VDR rs2228570 are not risk factors for reduced serum 25-OH vitamin D or vitamin D deficiency in patients with various forms of thyroid pathology patients in the West-Ukrainian population. Vitamin D levels were significantly lower in the carriers of AA and AG genotypes with hypothyroidism caused by autoimmune thyroiditis. In AA genotype carriers with postoperative hypothyroidism, 25-OH vitamin D levels were significantly lower compared to AA genotype carriers with autoimmune thyroiditis.
| S-EPMC8485381 | biostudies-literature
Project description:PurposeTo study the intake and sources of vitamin D and determinants of serum 25-hydroxyvitamin D (S-25(OH)D) in Finnish adolescents.MethodsWe studied 265 adolescents (117 girls) aged 15-17 years attending 8-year examinations of the PANIC Study, assessed diet using food records and other lifestyle factors by questionnaires, and analyzed S-25(OH)D by chemiluminescence immunoassay and determinants of S-25(OH)D using multivariate linear regression.ResultsMean (standard deviation) of total vitamin D intake from food and supplements was 19.2 (13.1) µg/d, and that of dietary vitamin D intake was 9.9 (5.4) µg/d. Milk fortified with vitamin D was the main dietary source of vitamin D, providing 45% of daily intake. Altogether, 29% of the adolescents used no vitamin D supplements and 25% did not meet the recommended total vitamin D intake of 10 µg/d. Mean (standard deviation) of S-25(OH)D was 62.0 (18.8) nmol/l, and S-25(OH)D was < 50 nmol/l in 29.5% of the adolescents. Vitamin D intake from supplements was the main determinant of S-25(OH)D (β = 0.465, p < 0.001), followed by consumption of milk products (β = 0.251, p < 0.001), consumption of meat products (β = 0.179, p = 0.002), travels to sunny countries (β = 0.178, p = 0.002), and average daylight time (β = 0.162, p = 0.004).ConclusionMost of the adolescents had vitamin D intake at the recommended level, although a fourth did not meet the recommended total vitamin D intake of 10 µg/d and almost a third had S-25(OH)D < 50 nmol/l. More attention should be paid to the sufficient intake of vitamin D in adolescents who do not use vitamin D supplements or fortified milk products.Trial registrationClinicalTrials.gov: NCT01803776, registered March 3, 2013.
| S-EPMC9941269 | biostudies-literature
Project description:Osteoporosis (OP) is often associated with other complications, such as impaired glucose homeostasis. Vitamin D deficiency is common and has been linked to bone metabolism and the regulation of blood sugar levels. The aim of this study was to evaluate the independent relationship between serum 25-hydroxyvitamin D (25[OH]D) and fasting blood glucose levels (FBG) in a group of patients diagnosed with OP. This is a retrospective cross-sectional study from a prospectively collected database at our tertiary referral center. Consecutive 2084 OP patients who were hospitalization were finally analyzed in this study. FBG is the dependent variable, serum 25(OH)D level of OP patients is exposure variable of this study. There was a linear significantly negative association between serum 25(OH)D and FBG (β, - 0.02; 95% CI - 0.03 to - 0.01; P = 0.0011) in the fully adjusted models. Specifically, when serum 25(OH)D level was less than 23.39 ng/mL, FBG decreased by 0.04 mmol/L for every 1 ng/mL increase of serum 25(OH)D level. When serum 25(OH)D was greater than 23.39 ng/ mL, the negative association was insignificant (P = 0.9616). If the association is confirmed, the clinical management of blood glucose in OP patients with serum 25(OH)D deficiency has instructive implications.
| S-EPMC10620140 | biostudies-literature
Project description:BACKGROUND:Few studies have prospectively examined the relationship between vitamin D status and prostate cancer risk in black men, a group at high risk for both low vitamin D status and prostate cancer. METHODS:Among black men in the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial, we identified 226 prostate cancer cases and 452 controls matched on age at randomization (±5 years), date of blood draw (±30 days), calendar year of cohort entry, and time since baseline prostate cancer screening (±1 year). Conditional logistic regression was used to estimate the odds ratios (ORs) and 95% confidence intervals (CIs) for the associations between serum 25-hydroxyvitamin D [25(OH)D], vitamin D binding protein (DBP), the 25(OH)D:DBP molar ratio, and prostate cancer risk. RESULTS:Serum 25(OH)D was not associated with overall prostate cancer (Q4 vs Q1: OR, 0.73; 95% CI, 0.40-1.33; P for trend = .25), although there were apparent inverse associations for nonaggressive disease (global P = .03, clinical stage I/II, and Gleason score <7) and among men ?62 years old (P for interaction = .04) that were restricted to Q3. Interestingly, serum DBP was significantly inversely associated with prostate cancer risk (Q4 vs Q1: OR, 0.45; 95% CI, 0.20-1.00; P for trend = .03), whereas the 25(OH)D:DBP molar ratio was not. Results were similar when we mutually adjusted for 25(OH)D and DBP, and we found no evidence of interaction between the two. CONCLUSION:Our study suggests higher (versus lower) circulating DBP may be independently associated with a decreased prostate cancer risk in black men independent of 25(OH)D status. Cancer 2017;123:2698-704. © 2017 American Cancer Society.
| S-EPMC5498231 | biostudies-literature