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Query: UNIPROT:P06889 (Mol)
 630,302 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The UK has insufficient intensity of sunlight at wavelengths 290-315 nm to enable cutaneous synthesis of vitamin D from October to April. There are regional differences in UVB strength throughout the UK but whether this translates to differences in vitamin D status is not known. We have reported seasonal variations in a cross-sectional study of over 3000 Scottish women in Aberdeen. The aim of this longitudinal study was to compare the seasonal variation of serum 25-hydroxyvitamin D [25(OH)D] in postmenopausal women residing in Aberdeen (57 degrees N) and Surrey (51 degrees N). Women attended 3-monthly visits over 12 months, starting summer 2006. In Aberdeen, 338 Caucasian women (mean age+/-SD, 61.7+/-1.5 years); and at Surrey, 138 Caucasian women (61.4+/-4.5 years) and 35 Asian women (59.9+/-6.4 years) had serum 25(OH)D measured by IDS enzyme immunoassay. In winter/spring none of the Caucasian women living in Surrey had 25(OH)D<20 nmol/L, but nearly a quarter of women in Aberdeen were vitamin D-deficient. This number decreased to 4.2% in summer/autumn. For the Asian women 17.1% were vitamin D-deficient in summer, increasing to 58.1% in winter. Using higher 25(OH)D deficiency cut-offs, the percentage of women affected was much higher. These longitudinal data show clear differences in vitamin D status between the north and south of the UK, and marked ethnic differences. They are consistent with our previous data and with cross-sectional data from the 1958 birth cohort. The low vitamin D status may have implications for bone health and other health outcomes, which is currently being investigated in this publication group. The extent of vitamin D deficiency in Asian women residing in the South of England is of concern.
J Steroid Biochem Mol Biol 2010 Jul
PMID:Seasonal 25-hydroxyvitamin D changes in British postmenopausal women at 57 degrees N and 51 degrees N: a longitudinal study. 2030 33

There is a lack of evidence that improving vitamin D status, without changing calcium intake, has a positive effect on bone turnover as indicated by bone marker changes. The objective was to measure the effect of vitamin D supplementation, in vitamin D deficient women (25(OH)D concentration<50 nmol/L), on osteocalcin (OC) and C-telopeptide (CTX). The study design was a randomised controlled intervention administering 4000 IU vitamin D3 or placebo daily for 6 months to South Asian women, aged>20 years. Subjects were stratified by age and menopausal status. Median (25th, 75th percentile) serum 25(OH)D increased significantly from 21 (11, 40) to 75 (55, 84) nmol/L with supplementation. In women>49 years or postmenopausal (n=26), who were not supplemented (n=13), CTX and OC levels increased (P=0.001, P=0.004 respectively), indicating an increased rate of bone turnover. With supplementation CTX decreased (P=0.012) and there was no significant change in OC. In women who were under 49 years and premenopausal (n=55; 29 supplemented), there was no significant response to supplementation in either CTX or OC. We conclude that correcting vitamin D deficiency in older women suppresses the age-induced increase in bone turnover and reduces bone resorption which would normally be exacerbated in conditions of low serum 25(OH)D.
J Steroid Biochem Mol Biol 2010 Jul
PMID:Vitamin D supplementation suppresses age-induced bone turnover in older women who are vitamin D deficient. 2030 51

Cardiovascular disease (CVD) is the leading cause of morbidity and mortality in patients with type 2 diabetes mellitus (T2DM). In type 2 diabetics, the prevalence of vitamin D deficiency is 20% higher than in non-diabetics, and low vitamin D levels nearly double the relative risk of developing CVD compared to diabetic patients with normal vitamin D levels. However, the mechanism(s) by which vitamin D deficiency leads to an increased susceptibility to atherosclerosis in these patients is unknown. We studied the effects of vitamin D replacement on macrophage cholesterol metabolism and foam cell formation in obese, hypertensive diabetics and non-diabetic controls. We found that 1,25-dihydroxy vitamin D3 [1,25(OH)2D3] suppressed foam cell formation by reducing acetylated low density lipoprotein (AcLDL) and oxidized low density lipoprotein (oxLDL) cholesterol uptake in diabetics only. 1,25(OH)2D3 downregulation of c-Jun N-terminal kinase activation reduced PPARgamma and CD36 expression, and prevented oxLDL-derived cholesterol uptake. In addition, 1,25(OH)2D3 suppression of macrophage endoplasmic reticulum stress improved insulin signaling, downregulated SR-A1 expression, and prevented oxLDL- and AcLDL-derived cholesterol uptake. The results of this research reveal novel insights into the mechanisms linking vitamin D signaling to foam cell formation in diabetics and suggest a potential new therapeutic target to reduce cardiovascular risk in this population.
J Steroid Biochem Mol Biol 2010 Jul
PMID:Vitamin D regulates macrophage cholesterol metabolism in diabetes. 2033 38

The objective of this work is to estimate the economic burden and premature death rate in Canada attributable to low serum 25-hydroxyvitamin D (25(OH)D) levels. Vitamin D deficiency has been linked to many diseases and conditions in addition to bone diseases, including many types of cancer, several bacterial and viral infections, autoimmune diseases, cardiovascular diseases, and adverse pregnancy outcomes. Canadians have mean serum 25(OH)D levels averaging 67 nmol/L. The journal literature was searched for papers reporting dose-response relationships for vitamin D indices and disease outcomes. The types of studies useful in this regard include randomized controlled trials, observational, cross-sectional, and ecological studies, and meta-analyses. The mortality rates for 2005 were obtained from Statistics Canada. The economic burden data were obtained from Health Canada. The estimated benefits in disease reduction were based on increasing the mean serum 25(OH)D level to 105 nmol/L. It is estimated that the death rate could fall by 37,000 deaths (22,300-52,300 deaths), representing 16.1% (9.7-22.7%) of annuals deaths and the economic burden by 6.9% (3.8-10.0%) or $14.4 billion ($8.0 billion-$20.1 billion) less the cost of the program. It is recommended that Canadian health policy leaders consider measures to increase serum 25(OH)D levels for all Canadians.
Mol Nutr Food Res 2010 Aug
PMID:An estimate of the economic burden and premature deaths due to vitamin D deficiency in Canada. 2035 22

Vitamin D deficiency is common among patients with myocardial diseases because sun-induced vitamin D production in the skin and dietary intake of vitamin D is often insufficient. Knockout mice for the vitamin D receptor develop myocardial hypertrophy and dysfunction. It has also been shown that children with rickets who suffered from severe heart failure could be successfully treated with supplementation of vitamin D plus calcium. In adults, almost all patients with heart failure exhibit reduced 25-hydroxyvitamin D levels, which are used to classify the vitamin D status. In prospective studies, vitamin D deficiency was an independent risk factor for mortality, deaths due to heart failure and sudden cardiac death. Several vitamin D effects on the electrophysiology, contractility, and structure of the heart suggest that vitamin D deficiency might be a causal factor for myocardial diseases. Data from interventional trials, however, are rare and urgently needed to elucidate whether vitamin D supplementation is useful for the treatment of myocardial diseases. In our opinion, the current knowledge of the beneficial effects of vitamin D on myocardial and overall health strongly argue for vitamin D supplementation in all vitamin D-deficient patients with or at high risk for myocardial diseases.
Mol Nutr Food Res 2010 Aug
PMID:Vitamin D deficiency and myocardial diseases. 2035 23

The allelic frequencies of apolipoprotein E (apoE) vary substantially around the world. There is a conspicuous south-to-north gradient of e4 frequencies in Europe, with the proportion of e4 carriers from only 10-15% in the south to 40-50% in the north. The mechanism may be related to the possibility that e4 carriers are less likely to develop vitamin D deficiency. In addition, Asian populations traditionally have lower e4 frequency than Europeans, which may be attributed in part to the scarce or irregular food supplies in Western world in the recent past. However, whether these geographical distribution gradients exist in China is yet unknown. ApoE genotypes of 200 children from Nanning City were determined by PCR-restriction fragment length polymorphism (RFLP) analysis. Allele frequency data of 18 other populations were collected from published sources and correlated with latitude and longitude information from different geographic resources. In our subjects, the frequencies of apoE genotypes were E3/E3: 73.0%, E3/E2: 15.0%, E4/E3: 5.0%, E4/E4: 5.0%, and E4/E2: 2.0%; the frequencies of apoE alleles were e2: 8.5%, e3: 83.0%, and e4: 8.5%, respectively. The total sample consisted of 3,679 individuals from 19 Chinese populations; the allelic frequencies were e2: 7.6%, e3: 85.5%, and e4: 6.9%, respectively; the proportion of e4 carriers was from 4.9% in Kunming to 17.5% in Harbin. Systemic comparison among multiple Chinese populations revealed that positive correlation existed between the e4 allele frequency distribution and latitude north (r=0.586, P=0.008), but no correlation of the e4 allele frequency distribution with longitude east was found (r=-0.018, P=0.942). We conclude that there is a south-to-north, but not an east-to-west gradient for the apoE4 allele in China.
Mol Biol Rep 2011 Jan
PMID:Does the geographical gradient of ApoE4 allele exist in China? A systemic comparison among multiple Chinese populations. 2035 5

This article gives an overview of the vitamin D status in Germany, provides evidence for an independent association of vitamin D deficiency with various chronic diseases, and discusses preventive measures for improving vitamin D status in Germany. The prevalence of vitamin D insufficiency is 40-45% in the general German population. An additional 15-30% are vitamin D deficient. Vitamin D can prevent falls and osteoporotic fractures in older people. There is also accumulating evidence that vitamin D may prevent excess mortality and may probably prevent some chronic diseases that occur in early life such as type 1 diabetes and multiple sclerosis. Adherence to present sun safety policy (avoidance of the sun between 11 am and 3 pm) and dietary recommendations (5-10 microg daily for adults) would, however, definitively lead to vitamin D deficiency. The estimated cost saving effect of improving vitamin D status in Germany might be up to 37.5 billion euro annually. It should be the goal of nutrition and medical societies to erase vitamin D deficiency in Germany within the next 5-10 years. To achieve this goal, the daily production of at least 25 microg of vitamin D in the skin or an equivalent oral intake should be guaranteed.
Mol Nutr Food Res 2010 Aug
PMID:The estimated benefits of vitamin D for Germany. 2037 91

We have previously shown that vitamin D deficiency in young male rats results in significant reduction in femoral trabecular bone volume (BV/TV). However, the effects of vitamin D deficiency and its impact on other relevant skeletal sites remain unclear. Ten week old male Sprague-Dawley rats were fed various levels of vitamin D3 (2, 4, 8, and 12 IU/day) with standard Ca (0.4%) until 30 weeks of age and achieved stable serum 25-hydroxyvitamin D3 (25D) levels between 16 and 117 nmol/L. At time of death, femora, L2 vertebrae and tibiae were processed for bone histomorphometric analyses and tibial cortical strength by 3-point mechanical testing. A significant association between serum 25D and trabecular bone occurred for both the distal femoral metaphysis (R2=0.34, P<0.05) and L2 vertebrae (R2=0.24, P<0.05). Tibia mid-shaft cortical bone was not, however, changed in terms of total volume, periosteal surface or endosteal surface as a function of vitamin D status. Furthermore, no changes to mechanical and intrinsic properties of the cortices were observed. We conclude that cortical bone is maintained under conditions of vitamin D deficiency in preference to cancellous bone in young growing rats.
J Steroid Biochem Mol Biol 2010 Jul
PMID:Discordant effects of vitamin D deficiency in trabecular and cortical bone architecture and strength in growing rodents. 2039 59

Vitamin D deficiency and PHPT are two common conditions, especially in postmenopausal women. Vitamin D deficiency is said to be even more frequent in PHPT patients than in the general population due to an accelerated conversion of 25OHD into calcitriol or 24-hydroxylated compounds. Although several studies have reported worsening of PHPT phenotype (larger tumours, higher PTH levels, more severe bone disease) when vitamin D deficiency coexists whereas vitamin D supplementation in PHPT patients with a serum calcium level<3 mmol/L has been shown to be safe (no increase in serum or urinary calcium) and to decrease serum PTH concentration, that many physicians are afraid to give vitamin D to already hypercalcemic PHPT patients. On the other hand, it is possible that, in some patients, a persistent vitamin D deficiency induces, in the long-term, an autonomous secretion of PTH (i.e. tertiary hyperparathyroidism). The mechanism by which this could occur is unclear however. Finally, as many, otherwise normal, subjects with vitamin D insufficiency may have an increased serum PTH level we believe that those with vitamin D insufficiency should be excluded from a reference population for serum PTH levels. By doing that, we found that the upper normal limit for serum PTH was 25-30% lower than in the whole population.
J Steroid Biochem Mol Biol 2010 Jul
PMID:Vitamin D and primary hyperparathyroidism (PHPT). 2039 61

Vitamin D deficiency is recognized as one of the most common chronic medical conditions in the world. Vitamin deficiency has been associated with increased mortality. The aim of the study here presented was to evaluate the vitamin D endocrine system (VDES) status in healthy blood donors and critically ill patients baseline and in response to treatment during a week with two doses of 1.5 mg of 25-hydroxyvitamin D3 and 2 microg calcitriol (1,25(OH)2D3) IV on alternate days, by monitoring levels in serum of major vitamin D metabolites in critically ill patients. Group 1: healthy blood donors (control group) (n=92), and group 2: critically ill subjects from an intensive care unit (ICU) (n=33). Critically ill patients were divided into three groups: group A (n=12) is the control group; group B (n=11), administration PO 1,5 mg of 25(OH)D3, in days 0 and 4 of treatment; and group C (n=11), administration IV of 2 microg 1,25(OH)2D3 on alternate days. Baseline serum levels of vitamin D2 and 25(OH)D2 were not detected. Vitamin D3 (9.8 vs 26.0 nM) (p<0.05), 25(OH)D3 (13.3 vs 52.3 nM) (p<0.001), and 1,25(OH)2D3 (53.8 vs 120.5 pM) (p<0.01) serum levels were significantly lower in critically ill subjects than in healthy donors. After treatment in group B: 25OHD3 increased to 46.0+/-16.5 ng/ml (p<0.0001) (22.2%<75 nM, 11.1% <50 nM). 1,25(OH)2D3 increased to 121.8+/-61.8 pM<0.01 whereas were slightly decreased in the other groups during the study. 24,25(OH)2D3 serum levels were increased in patients treated with calcitriol 8.5+/-5.3 vs 24.8+/-16.3 nM (p<0.05) while the levels kept stable in group A patients. In summary, critically ill patients have a severe vitamin D deficiency, which can be easily corrected by administration of high doses of 25OHD (PO). The VDES functional deficiency could be probably also corrected through administration of calcitriol (IV). Both treatments could produce an improvement in the general health and probably a reduction in overall mortality risk of the critically ill patients.
J Steroid Biochem Mol Biol 2010 Jul
PMID:Evaluation of vitamin D endocrine system (VDES) status and response to treatment of patients in intensive care units (ICUs) using an on-line SPE-LC-MS/MS method. 2039 67


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