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PubMed1982

Normal hepatic vitamin-D metabolism in icteric primary biliary cirrhosis associated with pronounced vitamin-D deficiency symptoms.

The intestinal absorption and hepatic metabolism of vitamin D were studied in a woman with icteric primary biliary cirrhosis (PBC) complicated by pronounced bone pain and muscle weakness due to vitamin-D deficiency. The patient had a markedly reduced intestinal absorption of vitamin D, while the 25-hydroxylation of this vitamin was found to be normal despite the presence of longstanding icterus. The malabsorption of fat-soluble compounds secondary to the cholestasis was probably further impaired by several years of cholestyramine treatment. Administration of 1.25-(OH)2D3 increased intestinal calcium absorption, normalized serum calcium and increased bone mineral content of the proximal tibia. Furthermore, drastic improvement of muscle weakness and relief of bone pain were observed. It is recommended that repeated measurements of serum 25-(OH)D should be carried out in patients with PBC, and especially in those treated with cholestyramine. In certain vitamin D deficient patients, studies using radio-labelled vitamin D may provide clinically valuable information as to the exact site of the underlying disturbances.

Cholestyramine Resin↗

PubMed1978

The effect of supplemental vitamin E on vitamin A serum levels in cystic fibrosis.

Effects of the ingestion of vitamin E with vitamin A on the serum levels of these vitamins and the urinary creatine to creatinine ratios of 18 children with cystic fibrosis disease of the pancreas (CF) was studied. After the daily ingestion for two months of a specially prepared capsule containing 5000 IU vitamin A palmitate and 100 mg d alpha-tocopherol acetate in aqueous dispersible form there was a significant increase in vitamin A as well as vitamin E levels of serum taken 3 1/2 hr postprandially. Creatine to creatinine ratios in single voiding of urine decreased.

Adolescent↗

PubMed1994

[Low serum vitamin B 12 level and vitamin B 12 deficiency in the elderly. When should supplement be provided?].

Low serum vitamin B12 levels and vitamin B12 deficiencies are frequently found in the elderly. The full syndrome of a vitamin B12 deficiency is rather simple to diagnose. The large applicability of the vitamin B12 assay also gives rise to many probably incomplete features. Low/low-normal vitamin B12 levels in screening procedures raise uncertainty whether this finding represents deficiency and should be followed by supplementation. In this paper the occurrence of low serum levels of vitamin B12 are discussed. To assess the clinical relevance of low/low-normal outcomes supplementary diagnostic procedures will be needed. Within this scope we illustrate the d.o.s.-test and the MMA-assay. Especially the latter will probably provide more answers to the treatment question. Systematic research is needed to clarify this issue. Meanwhile supplementation of all low and low-normal outcomes of the B12-assay seems the best answer.

Aged↗

PubMed2026

Vitamin D Deficiency During Pregnancy Is Associated With Greater LDL-C Increase, Elevated β-Hydroxybutyrate and Altered Neonatal Metabolic Markers-A Secondary, Pooled Analysis of the Randomized, Controlled Vitamin D and Lifestyle for Gestational Diabetes Prevention Trial (DALI).

INTRODUCTION: Vitamin D (vitD) plays a role in metabolic regulation, including lipid metabolism and insulin sensitivity. During pregnancy, profound physiological changes in lipid handling and ketogenesis occur to support fetal development. However, the extent to which maternal vitamin D status influences these metabolic adaptations and fetal metabolic markers remains unclear. METHODS: In this secondary analysis, we examined lipid distribution throughout pregnancy-from before 20 weeks' gestation to delivery-in women with overweight or obesity, stratified by vitamin D status (deficiency, insufficiency, or sufficiency), assessing both maternal and cord blood. Main inclusion criteria were: age > =18 years, singleton pregnancy, < 20 weeks' gestation, BMI ≥ 29 kg/m2. Women with GDM < 20 weeks' gestation were excluded. In total, 962 pregnant women were divided into vitD deficient (< 30 nmol/L, n = 102), insufficient (30-50 nmol/L, n = 222) and sufficient (> 50 nmol/L, n = 638) groups. VitD levels and lipid concentrations were assessed at < 20, 24-28 and 35-37 weeks' gestation and in cord blood. RESULTS: Compared with vitD sufficient women, women with vitD deficiency had significantly larger increases in LDL-C throughout pregnancy and ß-OH-butyrate at 24-28 weeks' gestation, in adjusted analysis. VitD in cord blood was highest in offspring of mothers with vitD sufficiency. In cord blood, significantly higher ß-OH-butyrate was observed with vitD deficiency; lipid concentrations were similar between groups. CONCLUSIONS: Early vitamin D deficiency before 20 weeks of gestation was associated with altered metabolic trajectories during pregnancy, including greater increases in LDL cholesterol and ketone body concentrations in women with overweight or obesity, as well as higher cord blood ketone levels in their offspring. These findings suggest that early maternal vitamin D status may influence maternal and fetal metabolic adaptations, although causal relationships and clinical implications require further investigation. TRIAL REGISTRATION: Trial registered at ISRCTN registry (https://doi.org/10.1186/ISRCTN70595832) trial number ISRCTN70595832. Registration date 02/12/2011.

Humans↗

PubMed1998

Simultaneous determination of fat-soluble vitamins A, D and E and pro-vitamin D2 in animal feeds by one-step extraction and high-performance liquid chromatography analysis.

Traditionally, alkaline saponification for the extraction of vitamins and step-wise HPLC analyses have been widely used for analysis of fat-soluble vitamins in animal feeds. The objective of present study was to develop an analytical method using one-step extraction and simultaneous determination of the vitamins A, D and E and pro-vitamin D2 in animals feeds b HPLC. Various analytical conditions were tested which included sample particle size extraction solvents, the ratio of solvent to sample, extraction approach, extraction time, N2 protection, prepurification with Sep-Pak cartridge and detection wavelength. The accuracy of the developed method has been proven by comparison with the AOAC method. The reproducibility of the developed method has been substantiated by repeated recovery experiments. The detection limit for the four vitamins was 10 ng/g of feed sample. One of the important properties of the present method is rapidity and ease of use.

Animal Feed↗

PubMed1998

Induction of prothrombin synthesis by K-vitamins compared in vitamin K-deficient and in brodifacoum-treated rats.

Vitamin K is a group name for a number of prenylated 2-methyl-1,4-naphtoquinones, which may differ in their ability to function as a cofactor for prothrombin biosynthesis. To quantify the bioactivity of different forms of vitamin K, two experimental animal systems are frequently used: vitamin K-deficient rats and anticoagulated rats. In this paper both models are compared, and it is shown that the results obtained depend on the model used. The main reason for this discrepancy is the difference in recycling of vitamin K-epoxide, which results in a 500 times higher vitamin K requirement in anticoagulated rats. Absorption and hepatic accumulation of long chain menaquinones seem to be restricted to a maximum, whereas also the lipophilic nature of long chain menaquinones may hamper the quinone-quinol reduction in anticoagulated animals. If these data may be extrapolated to patients, food items rich in K1 and MK-4 would be expected to influence the stability of oral anticoagulation to a much larger extent than food items primarily containing higher menaquinones.

4-Hydroxycoumarins↗

PubMedDate not supplied

Maternal trace elements, vitamin B12, vitamin A, folic acid, and fetal malformations.

The demonstrated teratogenicity of maternal zinc deficiency in rats has led to burgeoning interest in zinc and other trace elements as important factors in embryonic development. Levels of zinc, copper, manganese, magnesium, folic acid, vitamin B12 and vitamin A were evaluated at the beginning of pregnancy in the plasma of pregnant women who later delivered a malformed newborn. Fetal chromosomal anomalies and recognizable nonchromosomal syndromes were excluded. The results were compared to control women who delivered normal babies. One hundred seventy mothers had malformed children. The more frequent congenital malformations were congenital heart diseases (72 cases including 24 VSD), musculoskeletal malformations (21 cases), urogenital malformations (23 cases), spina bifida (6 cases), hydrocephaly (6 cases), and labial cleft (14 cases). Maternal plasma concentrations of zinc, copper, magnesium, manganese, folate, vitamin B12, and vitamin A of malformed children did not differ from controls. Thus vitamin profiles do not form a suitable means for identifying women at risk for having a child with congenital malformations.

Congenital Abnormalities↗

PubMed1981

Vitamin K-dependent carboxylase. Stoichiometry of carboxylation and vitamin K 2,3-epoxide formation.

Crude rat liver microsomal preparations catalyze a reduced vitamin K- and oxygen-dependent carboxylation of peptide-bound glutamyl residues to gamma-carboxyglutamyl residues. The same preparations convert reduced vitamin K to its 2,3-epoxide. The stoichiometry of this relationship has been investigated. At saturating concentrations of CO2, equal amounts of vitamin K 2,3-epoxide and gamma-carboxyglutamic acid are formed. As the CO2 concentration is lowered, this ratio shifts to a large excess of epoxide. Alterations in glutamyl substrate concentration or Mn2+ concentration cause equal alterations in both activities, while addition of KCN stimulated epoxidation and inhibited carboxylation. The release of 3H from a gamma-[3H]glutamyl substrate was tightly coupled to epoxide formation, and both of these activities were inhibited by glutathione peroxidase. These data are consistent with a reaction mechanism in which an oxygenated form of vitamin K activates the substrate glutamyl residue by hydrogen removal in a reaction that is coupled to vitamin K epoxide formation.

Animals↗

PubMed1981

Localization of tritiated vitamin A in lymph nodes of the mouse: an autoradiographic study of vitamin A-storing cells.

Localization of tritiated vitamin A in lymph nodes of the mouse was investigated by the use of light- and electron-microscopic autoradiography. Young male mice were fed a diet containing 3H-vitamin A acetate for a week. Lymph nodes were removed and prepared for autoradiography. Lipid droplets in fibroblast-like cells showed high concentrations of radioactivity. These cells were distributed around lymphatic sinuses and blood vessels. The cells can, therefore, be classified as "vitamin A-storing cells" according to criteria proposed earlier by Yamada and Hirosawa (1976). Control animals from the same litter were maintained on ordinary laboratory food for the same period and examined by electron microscopy. Lipid-droplet-containing cells were found in the same areas as in the experimental animals but in fewer numbers. This suggests that the increased number of vitamin A-containing lipid droplets is due to hypervitaminosis A in the experimental animals. The presence of some cells containing these droplets in the control animals would imply that even under normal feeding conditions the animals ingested excess amounts of vitamin A, which was retained in lipid droplets. The stored vitamin A probably participates in metabolic processes such as the formation of glycoproteins in ground substance.

Animals↗

PubMed2006

Associations between vitamin D, vitamin D receptor gene and the androgen receptor gene with colon and rectal cancer.

The transcriptional activity of the vitamin D receptor (VDR) gene is regulated, at least in part, by the androgen receptor (AR) gene. We evaluate how the number of polyglutamine (CAG) repeats of the AR gene influence colorectal cancer in conjunction with vitamin D, sunshine exposure and VDR. Studies of colon (1,580 cases and 1,968 controls) and rectal (797 cases and 1,016 controls) cancer were used. Vitamin D intake and average hours of sunshine exposure interacted with AR genotype in men. Men with low vitamin D intake or low levels of sunshine exposure who had 23+ CAG repeats of the AR gene had the greatest risk of colon cancer. ORs for men with 23 or more CAG repeats of the AR gene and in the lowest tertile of vitamin D intake or sunshine exposure were 1.71 (95% CI 1.14, 2.56) and 1.51 (95% CI 1.09, 2.09). Men with high levels of sunshine exposure were at reduced risk of developing rectal cancer if they had 23 or more CAG repeats (OR 0.62 95% CI 0.39, 0.97) than if they had fewer than 23 CAG repeats. The FF genotype of the Fok1 VDR gene was associated with reduced risk of colon cancer among women with any allele of 23+ CAG repeats (OR 0.62 95% CI 0.44, 0.88), whereas men with the LL/bb VDR genotypes were at reduced risk of rectal cancer if they also had 23+ CAG repeats (OR 0.71 95% CI 0.48, 1.05) relative to men with fewer than 23 CAG repeats of the AR gene. These data provide support for the role of vitamin D and sunshine exposure in the etiology of colorectal cancer and suggest that AR gene may modulate the association.

Adult↗

PubMed1998

Effect of 25-OH-vitamin D on fracture healing in elderly rats.

To investigate the effect of 25-OH-vitamin D supplements (calcidiol) on fracture healing in the elderly, an experimental model with 15 18-month-old female Wistar rats was designed. An experimental fracture in the middle third of both femora of each rat was made. Then the rats were randomly assigned to two groups: one group was subcutaneously treated with 25-OH-vitamin D during all healing processes, and the other group (the control group) was not. After 5 weeks of healing, the animals were killed and both femora were extracted. Blood samples were collected before fracture and at death to determine the levels of 25-OH-vitamin D. All bones that were extracted were subjected to a torsion test to assess healing; a significantly greater maximum shear force before failure was supported in the treated group (p < 0.01). Moreover, a positive correlation (p < 0.01; r=0.55) was found between blood levels of 25-OH-vitamin D at death and the mechanical strength of the callus. Thus, the administration of 25-OH-vitamin D after the experimental fracture significantly improved the mechanical strength of the fractured bone. If similar results are found in the human, then treatment with 25-OH-vitamin D after the occurrence of a fracture would be a good way to improve fracture healing in the elderly.

Aging↗

PubMed1980

Treatment of hypophosphataemic vitamin D-resistant rickets and adult presenting hypophosphataemic vitamin D-resistant osteomalacia.

The results of the treatment of 12 patients with hypophosphataemic vitamin D-resistant rickets, 4 similar patients who were first diagnosed in adulthood, and 2 adult patients with hypophosphataemic vitamin D-resistant osteomalacia are presented. Treatment with a high dosage of Vitamin D2 was begun between 1 1/2 and 7 years of age. The dose of Vitamin D2 required for the treatment of rickets varied widely depending on the severity of the process and the age of the patient. Four patients with leg deformities required osteotomy or other operations. In other patients deformities improved with medical treatment alone. Dwarfism and severe deformity of the legs were characteristic features in rickets first diagnosed in adulthood. Radiographic features were Looser's zones, a coarse trabecular pattern, increased bone density and ligamentous calcification. These patients presented several difficult orthopaedic problems. Two brothers with hypophosphataemic vitamin D-resistant osteomalacia presented with bone pains, muscle weakness, limitation of motion in the back and height loss. Treatment with oral phosphate supplements in addition to high doses of Vitamin D2 was dramatic, with complete disappearance of muscle weakness and bone pain.

Adolescent↗

PubMed1981

Clinical evaluation of simultaneously administered 58Co labelled vitamin B12 and 57Co labelled vitamin B12 bound to intrinsic factor in patients with pernicious anaemia.

The clinical and laboratory data from 75 patients with altered vitamin B 12 absorption were reviewed. In 36 cases the diagnosis of pernicious anaemia had been established. Of these, 14 patients showed malabsorption of radiolabelled vitamin B 12, but the absorption of vitamin B 12 bound to the intrinsic factor (IF) was normal (Group A). The other 22 patients with pernicious anaemia showed altered free and IF-bound vitamin B 12 absorption (Group B). Laboratory and clinical data and the absorption tests (xylose and fat excretion) were more abnormal in group B than in group A. Finally, 39 patients (Group C) with general malabsorption showed alternation of the absorption of free and IF-bound vitamin B 12 (Group C). The clinical nd biological data were different in these patients from that found in groups A and B. It is possible that in patients with pernicious anaemia who are untreated an alteration of the intestinal mucosa may produce a malabsorption of vitamin B 12 even in the presence of intrinsic factor.

Anemia, Pernicious↗

PubMed1987

Vitamin D toxicity complicating the treatment of senile, postmenopausal, and glucocorticoid-induced osteoporosis. Four case reports and a critical commentary on the use of vitamin D in these disorders.

Hypervitaminosis D developed in four patients with osteoporosis or osteomalacia. All patients were given pharmacologic doses of vitamin D, had reduced baseline levels of renal function, and became hypercalcemic with acute renal failure. Measured 25-hydroxyvitamin D (25-OH D) levels were elevated in three patients; levels were not determined in a fourth patient who became normocalcemic when vitamin D therapy was discontinued. Published data on the use of vitamin D for prophylaxis or treatment of any form of osteoporosis fail to document benefits superior to those of calcium alone or calcium with estrogens and fluoride. Data on the use of 25-OH D show no greater benefit than for vitamin D. The use of 1,25-dihydroxyvitamin D (1,25-OH2 D) plus calcium may be superior to the use of calcium alone in some forms of osteoporosis. Vitamin D toxicity is associated with enhanced resorption of bone in some patients. Morbidity included extended hospitalization, dialysis, and chronic renal failure. Pharmacologic doses of vitamin D cannot be recommended for any form of osteoporosis.

Acute Kidney Injury↗

PubMed1984

Pancreatic vitamin D-dependent calcium binding protein: biochemical properties and response to vitamin D.

The biochemical properties of a chick pancreatic calcium binding protein (CaBP) and its response to vitamin D status and dietary calcium and phosphorus levels were studied and compared with the known vitamin D-dependent CaBPs present in the chick intestine and kidney. Pancreatic CaBP is homologous to the intestinal CaBP on the basis of immunological cross-reactivity, molecular size (28,200 Da), and charge properties (chromatographic mobility on DEAE-Sephadex in the presence of either EDTA or Ca2+). Pancreatic levels of CaBP respond to changes in vitamin D status and dietary Ca and P level in a fashion similar to the intestinal CaBP. Thus, in the absence of dietary vitamin D, both pancreatic and intestinal CaBPs were essentially undetectable, while in the presence of dietary vitamin D, a low dietary P (0.05%) elevated the pancreatic and intestinal CaBP 1.5X and 1.6X, respectively, compared to the CaBP levels present with normal dietary Ca and P (1.0%, 1.0%). The tissue levels of pancreatic CaBP (6-10 ng/mg protein) are about 0.2% of the intestine (5000 ng/mg protein) and 1% of the kidney CaBP (700 ng/mg protein). However, when corrections are made for the CaBP distribution in the tissues and expressed as CaBP concentration per CaBP-containing cells, the pancreatic CaBP level was 30% of the intestine and 10% of the kidney. Collectively, these results suggest that the chick pancreatic vitamin D-dependent CaBP is a homologous protein to the intestinal CaBP, both with regards to its relative cellular concentration as well as in its response to changing dietary levels of Ca and P.

Animals↗

PubMed1984

Skin calcium-binding protein: effect of vitamin D deficiency and vitamin D treatment.

The amount of skin calcium-binding protein, evaluated using a sensitive radioimmunoassay and indirect immunofluorescence, was decreased in vitamin-D deficient rats and increased after one week vitamin D3 or 1 alpha-hydroxyvitamin D3 treatment. In vitamin D replete and in vitamin D-deficient animals, skin calcium-binding protein was not sensitive to changes in dietary and/or serum calcium concentrations. These results indicate that this protein is different from other calcium-binding proteins such as parvalbumin and calmodulin which are not vitamin D-dependent, and also different from intestinal calcium-binding protein which, in D replete animals, is sensitive to changes in dietary and serum calcium concentrations. Skin calcium-binding protein may, therefore, represent a new class of vitamin D-dependent protein.

Animals↗

PubMed1978

Formation of vitamin D metabolites from 3H- and 14C-radiolabelled vitamin D-3 in chronic liver diseases.

Four of the eight patients studied were vitamin D replete and 4 vitamin D depleted as judged by serum 25-hydroxy vitamin D (25-OHD) concentration. Three of the 4 vitamin D depleted patients (including 2 with histological osteomalacia) formed radioactive 1,25-dihydroxycholecalciferol. One of the four vitamin D replete patients formed 1,25-dihydroxycholecalciferol but all formed 24,25-dihydroxycholecalciferol. This study suggests that patients with liver disease form dihydroxy vitamin D metabolites in an appropriate manner.

Adult↗

PubMed1991

Vitamin D and chick embryonic yolk calcium mobilization: identification and regulation of expression of vitamin D-dependent Ca2(+)-binding protein, calbindin-D28K, in the yolk sac.

The developing chick embryo acquires calcium from two sources. Until about Day 10 of incubation, the yolk is the only source; thereafter, calcium is also mobilized from the eggshell. We have previously shown that during normal chick embryonic development, vitamin D is involved in regulating yolk calcium mobilization, whereas vitamin K is required for eggshell calcium translocation by the chorioallantoic membrane. We have studied here the biochemical action of 1,25-dihydroxy vitamin D3 in the yolk sac by examining the expression and regulation of the cytosolic vitamin D-dependent calcium-binding protein, calbindin-D28K. Two types of embryos are used for this study, normal embryos developing in ovo and embryos maintained in long-term shell-less culture ex ovo, the latter being dependent solely on the yolk as their calcium source. Our findings are (1) calbindin-D28K is expressed in the embryonic yolk sac, detectable at incubation Days 9 and 14; (2) the embryonic yolk sac calbindin-D28K resembles that of the adult duodenum in both molecular weight (Mr 28,000) and isoelectric point, as well as the presence of E-F hand Ca2(+)-binding structural domains; (3) systemic calcium deficiency caused by shell-less culture of chick embryos results in enhanced expression of calbindin-D28K in the yolk sac during late development; (4) yolk sac calbindin-D28K expression is inducible by 1,25-dihydroxy vitamin D3 treatment in vivo and in vitro; and (5) immunohistochemistry revealed that yolk sac calbindin-D28K is localized exclusively to the cytoplasm of the yolk sac endoderm. These findings indicate that the chick embryonic yolk sac is a genuine target tissue of 1,25-dihydroxy vitamin D3.

Animals↗