Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “VITAMINS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 847 records · Page 47Linked to original sources
PubMed2005

Vitamin D repletion in patients with primary hyperparathyroidism and coexistent vitamin D insufficiency.

Vitamin D insufficiency is common in patients with primary hyperparathyroidism (PHPT) and may be associated with more severe and progressive disease. Uncertainty exists, however, as to whether repletion of vitamin D should be undertaken in patients with PHPT. Here we report the effects of vitamin D repletion on biochemical outcomes over 1 yr in a group of 21 patients with mild PHPT [serum calcium <12 mg/dl (3 mmol/liter)] and coexistent vitamin D insufficiency [serum 25 hydroxyvitamin D [25(OH)D] <20 microg/liter (50 nmol/liter)]. In response to vitamin D repletion to a serum 25(OH)D level greater than 20 microg/liter (50 nmol/liter), mean levels of serum calcium and phosphate did not change, and serum calcium did not exceed 12 mg/dl (3 mmol/liter) in any patient. Levels of intact PTH fell by 24% at 6 months (P < 0.01) and 26% at 12 months (P < 0.01). There was an inverse relationship between the change in serum 25(OH)D and that in intact PTH (r = -0.43, P = 0.056). At 12 months, total serum alkaline phosphatase was significantly lower, and urine N-telopeptides tended to be lower than baseline values (P = 0.02 and 0.13, respectively). In two patients, 24-h urinary calcium excretion rose to exceed 400 mg/d, but the group mean 24-h urinary calcium excretion did not change. These preliminary data suggest that vitamin D repletion in patients with PHPT does not exacerbate hypercalcemia and may decrease levels of PTH and bone turnover. Some patients with PHPT may experience an increase in urinary calcium excretion after vitamin D repletion.

Adult↗
PubMed1988

Vitamin K reversible hypoprothrombinemia in rats. II. Efficacy of vitamin K on latamoxef-induced coagulopathy in rats.

Feeding of a vitamin K-deficient diet caused the development of hypoprothrombinemic changes in rats such as prolongation of prothrombin time (PT) and activated partial thromboplastin time (APTT), decreases in plasma prothrombin and clotting factor VII levels, and an increase in the descarboxyprothrombin (PIVKA) level in both plasma and liver. Successive administrations of latamoxef (LMOX) to the vitamin K-deficient rats resulted in the further enhancement of these changes. After the development of hypoprothrombinemia with LMOX, a single subcutaneous injection of vitamin K1 normalized most of these abnormalities in blood coagulation parameters within 6 hr. When vitamin K was given at 200 micrograms/kg, PT, APTT and the plasma PIVKA level showed normal values for at least 8 days even when the animals were fed a vitamin K-deficient diet and treated with LMOX during the recovery period. The amount of vitamin K required to maintain most of the blood coagulation parameters in the normal range was about 3 micrograms/kg/day. The plasma level of vitamin K was higher than 0.3-0.5 ng/ml when the blood coagulation parameters were maintained in the normal range.

Animals↗
PubMed1990

Enrichment of the stages of the seminiferous epithelium in vitamin A-replaced-vitamin A-deficient rats.

Morphometric study revealed that, at 40 days after the start of vitamin A replacement, A1 spermatogonia and preleptotene spermatocytes appeared in more than 70% of the whole mounts of seminiferous tubules of vitamin A-deficient rats. By 42 days, the appearance of these cell types was reduced by 50%, and A2 and A3 spermatogonia were predominant. By 46 days, A1-A3 spermatogonia appeared in less than 30% of the tubular length while A4, intermediate and B spermatogonia became the major cell types in the basement compartment of seminiferous tubules. The predominance of spermatogonia noted at given times was corroborated by higher frequencies of tubular cross-sections of stages in which that particular type of spermatogonium resides. These results indicate that seminiferous tubules of vitamin A-replaced-vitamin A-deficient rats are 'enriched' for particular stages. Tracing the development of [3H]thymidine-labelled preleptotene spermatocytes revealed normal kinetics of germ cell differentiation in these animals. Furthermore, the spermatogonial proliferations in the vitamin A-replaced-vitamin A-deficient rats were quantitatively normal. We suggest that vitamin A replacement may result in temporal suppression of the differentiation of A2-B spermatogonia, leading to a stimulation or synchronization of certain groups of undifferentiating spermatogonia which undergo active proliferation simultaneously. These synchronized populations of spermatogonia continue to proliferate and differentiate, thus resulting in the stage-enrichments noted at later times.

Animals↗
PubMed1983

Influence of dietary fiber (konjac mannan) on absorption of vitamin B12 and vitamin E.

The subjects of this study were six normal and five maturity onset diabetics. On the first day of the study, subjects were given a control test meal, prepared by adding vitamin B12 3000r (mecobalamin) and vitamin E 500 mg (tocopherol acetate), after a 12-hr overnight fast. Then, on the second day in the case of the normal subjects, and on the seventh day in the case of the diabetic subjects, the subjects received a second test meal with 3.9 g konjac mannan (glucomannan). Venous blood samples were taken immediately before the test meal and again after 1, 3, 5, 8, 12 and 24 hr for analysis of vitamins. The absorption rate of vitamin E into the intestine was reduced when konjac mannan was added to the test meals, but that of vitamin B12 was not reduced in normal or diabetic subjects. It is suggested that konjac mannan reduces fat-soluble vitamin absorption removing bile acids, but does not reduce fat-insoluble vitamin absorption in the intestine.

Adult↗
PubMed2006

The problem of low levels of vitamin D and osteoporosis: use of combination therapy with alendronic acid and colecalciferol (vitamin D3).

Osteoporosis and fragility fractures are common in the elderly population and represent a large public health burden. Non-pharmacological recommendations for the management of osteoporosis include modification of lifestyle behaviours, increased weight-bearing exercise and consumption - through dietary or supplement sources - of adequate amounts of calcium and vitamin D. Although current guidelines include recommendations on calcium and vitamin D intake, patients frequently do not take sufficient amounts, even when supplements are provided free of charge. Vitamin D is essential for mineral metabolism, and low levels are associated with impaired skeletal metabolism and neuromuscular function. Nutritional sources of vitamin D are limited, and supplementation is usually necessary. A high prevalence of low vitamin D levels has been reported in a number of populations worldwide, including women being treated for osteoporosis and those with fragility fractures. At present, bisphosphonates are the most commonly prescribed pharmacological treatments for osteoporosis, and alendronic acid is the most frequently prescribed bisphosphonate. A nitrogen-containing bisphosphonate, alendronic acid has demonstrated anti-fracture efficacy at vertebral and non-vertebral skeletal sites, including the hip, in addition to long-term safety and efficacy. Weekly administration of alendronic acid takes advantage of the pharmacokinetics of the drug and osteoclast biology to optimise treatment, and may improve patient adherence. Combining alendronic acid 70mg and colecalciferol (vitamin D(3)) 2800 IU in a single, once-weekly tablet has the advantage of combining the proven efficacy of an established bisphosphonate, alendronic acid, with the amount of vitamin D currently recommended for osteoporosis management.

Alendronate↗
PubMed1986

Serum concentrations of vitamin D metabolites in vitamin D supplemented pregnant women. A longitudinal study.

The serum concentrations of the vitamin D metabolites 25-OHD, 1,25-(OH)2D, 24,25-(OH)2D and 25,26-(OH)2D, and of vitamin D binding protein (DBP), were determined longitudinally in 22 vitamin D supplemented pregnant women, and in 17 age-matched non-pregnant women studied during the summer. The pregnant women had higher 25-OHD and 1,25-(OH)2D, similar 24,25-(OH)2D, and lower 25,26-(OH)2D concentrations than the non-pregnant group. The relative concentrations of 24,25-(OH)2D and 25,26-(OH)2D (expressed as the molar ratio of these metabolites to 25-OHD) were lower during pregnancy. The DBP levels were increased in pregnancy, but the calculated free fraction (i.e. not bound to DBP) of the hormonal form of vitamin D, 1,25-(OH)2D, was still persistently higher in the pregnant than in the non-pregnant women. The study suggests that a daily vitamin D supplement of 400 IU satisfies the vitamin D requirement of pregnant women living in a cool climate with limited sun exposure. The increased absolute and relative concentration of 1,25-(OH)2D and decreased relative levels of 24,25-(OH)2D and 25,26-(OH)2D further suggest that the increased intestinal calcium and phosphate absorption, which is known to occur during pregnancy, is at least partially mediated by the vitamin D endocrine system.

24,25-Dihydroxyvitamin D 3↗
PubMed2000

Intestinal, hepatic, and circulating vitamin K levels at low and high intakes of vitamin K in rats.

The aim of the present study was to assess how high doses of dietary vitamin K influence the intestinal profile of K-vitamins in vitamin K-deficient rats, and whether the induced changes are reflected in the hepatic vitamin K store. Vitamin K-deficient rats were fed for 10 d on diets containing different forms of vitamin K, and it was determined how these diets affected the vitamin K concentration at various sites of the instestine, serum, and the liver. It was found that the absorption of phylloquinone from standard food is not more than 10%, while the absorption of pharmacological doses of oil-solubilized phylloquinone and menaquinone-4 was also far from complete (18 and 55% respectively). High intakes of phylloquinone suppress the colonic production of all higher menaquinones. High menaquinone-4 intake induces very high menaquinone-8 concentrations, both in the colonic contents as well as in the liver. These data suggest that menaquinone-4 may be converted into menaquinone-8 (but not into other menaquinones) via a metabolic pathway which has not been reported previously.

Absorption↗
PubMed1976

The differential effects of chemical carcinogens on vitamin A status and on microsomal drug metabolism in normal and vitamin A-deficient rats.

Male Sprague-Dawley rats were maintained on a vitamin A-deficient diet for 5 weeks. Although serum and hepatic levels of vitamin A were significantly lower at this time, no outward signs of vitamin A deficiency were present. Hepatic microsomal levels of cytochrome P-450 in the vitamin A-deficient animals were 70% that of the control animals. Of the three microsomal enzymes studied, ethylmorphine N-demethylase, aniline hydroxylase, and aminopyrine N-demethylase, only the last one was adversely affected by vitamin A deficiency. 3-Methylcholanthrene, phenobarbital, and 2-acetylaminofluorene had a greater inductive effect and cytochrome P-450 in vitamin A-deficient rats. 4-Dimethylaminoazobenzene treatment decreased in the level of cytochrome P-450 in control rats more than in deficieny rats. The hepatic concentration of vitamin A was significantly reduced in control rats that were given injections of 3-methylcholanthrene, 2-acetylaminofluorene, or phenobarbital. Benzo(a)pyrene and 4-dimethylaminoazobenzene had less effect.

Aminopyrine↗
PubMed2005

Incidental finding of vitamin-D deficient rickets in an otherwise healthy infant--a reappraisal of current vitamin-D supplementation guidelines.

In an effort to prevent rickets and vitamin-D deficiency in healthy infants, the American Academy of Pediatrics recommends a supplement of 200 IU per day of vitamin D to all breastfed and nonbreastfed infants unless they consume at least 500 ml per day of vitamin-D-fortified formula or milk. Case reports of infantile vitamin-D-deficient rickets secondary to maternal vitamin-D deficiency have been reported but focused on mothers who had predictable risk factors for such a deficiency. We report on an infant with vitamin-D-deficient rickets who did not have nutritional risk factors and whose mother did not have nutritional or medical risk factors for such a deficiency. We conclude that the current vitamin-D supplementation guidelines be extended to all infants, regardless of feeding volume or source, or at least to all infants born to dark-skinned mothers.

Diagnosis, Differential↗
PubMed1990

[The role of vitamin E in metabolism and reception of vitamin D].

It was found that calcium exchange disturbances under vitamin E deficiency is due to changes in the metabolism of vitamin D. In vitamin E-deficient rats the serum blood levels of hydroxyvitamin D (25-OHD) showed no significant changes, whereas the concentration of the hormonal form of 1.25-hydroxyvitamin D [1.25(OH)2D], decreased by 40%. In vitro studies showed that the 25-hydroxylase D3 activity in the livers of rats with E-avitaminosis had a tendency to decrease (by 22%), whereas that of 24-hydroxylase dropped drastically (by 52%). The serum blood levels of the parathyroid hormone (PTH) and kidney levels of cAMP under E-avitaminosis were significantly lowered. Preincubation of kidney slices with the adenylate cyclase activator, forskolin, increased the activity of 1-OHase in about the same degree as that in vitamin E-rich rats. The free radical scavenger, BHT, added to kidney slices suppressed the activity of the both enzymes; this finding testifies to the low O2-binding affinity of these monooxygenases. The content of 1.25(OH)2D3 receptors occupied in vivo in the kidneys of vitamin E-deficient rats decreased 2.5-fold; however, the binding of 1.25(OH)2D3-receptor complexes to heterologous DNA was unaffected thereby. The vitamin deficiency in vivo results in the inhibition of vitamin D metabolism in the liver and kidney concomitant with the formation of active metabolites and decreases the concentration of hormone-receptor complexes in target tissues.

Animals↗
PubMed1989

Vitamin D status and concentrations of serum vitamin D metabolites and osteocalcin in elderly patients with femoral neck fracture: a follow-up study.

Vitamin D status and the serum osteocalcin concentration in patients with femoral neck fractures were studied as follows. Thirty-seven elderly patients (P) with fracture of the femoral neck were studied, whereas 24 age-matched persons (C) seen at the out-patient department for non-orthopaedic reasons served as controls. The dietary intake of vitamin D, estimated using a vitamin D score based on food items known to be the main sources of vitamin D, was significantly lower in the patients than in the controls. There was no difference in the serum 25-hydroxy-vitamin D (25-OH-D) (P: 22.3 +/- 7.5 nmol/l; C: 27.5 +/- 13.5) or the serum 1,25-dihydroxy-vitamin D3 concentration (P: 86 +/- 43 pmol/l; 31) C: 85 +/- 31) between the groups. The 25-OH-D concentration was, however, low as compared to reference values, suggesting vitamin D deficiency in both groups. There was no difference in the serum osteocalcin concentration between the groups (P: 3.1 +/- 1.7 micrograms/l; C: 3.4 +/- 1.5). One year later the serum osteocalcin concentrations (5.9 +/- 2.2 micrograms/l, n = 11) was significantly higher (P less than 0.005) in the patients than at the time of the fracture (3.2 +/- 2.2 micrograms/l), indicating an active bone turnover in the patients still present 1 year after the fracture.

Aged↗
PubMed1985

[Vitamin A and vitamin E in dermatology].

Vitamin A is necessary to maintain the integrity and the differentiation of epithelia of the skin and adnexa. Evident deficiency of vitamin A in chronic diseases, malabsorption and liver affections may result in skin xerosis, follicular keratosis, and metaplasia of mucous membranes. The remarkable toxicity of vitamin A in high doses does not recommend its usage in dermatology. On the contrary the employ of retinoids, synthetic derivatives of vitamin A, brings to excellent results. These vitamin A compounds are much more effective, even if they show important side-effects. Etretinate and isotretinoin are widely used in psoriasis, keratinization disorders, and severe acne. Vitamin E functions in skin biology are not totally known. Vitamin E is used in the treatment of dermolytic recessive epidermolysis bullosa, with controversial results.

Dermatology↗
PubMed1993

Restoration of tissue antioxidants and prevention of renal stone deposition in vitamin B6 deficient rats fed with vitamin E or methionine.

Observed loss in body weight gain, increased lipid peroxidation reaction, decreased concentrations of antioxidants, ascorbic acid, alpha-tocopherol and reduced glutathione and antioxidant enzymes, glutathione peroxidase and catalase and increased concentration of hydroperoxides and hydroxyl radicals in vitamin B6 deficient rat liver [J Nutri Biochem, 2 (1991) 245] and kidney [Biochem International, 21 (1991) 599] were nearly normalized on feeding with vitamin E or methionine. Accumulation of oxalate and calcium during vitamin B6 deficiency was abolished by feeding vitamin E or methionine. Calcium oxalate deposition observed in vitamin B6 deficient kidney was completely prevented when fed along with vitamin E or methionine. However the hyperoxaluria and hypercalciuria persisted even after feeding with vitamin E or methionine.

Animals↗
PubMed2006

The classic receptor for 1alpha,25-dihydroxy vitamin D3 is required for non-genomic actions of 1alpha,25-dihydroxy vitamin D3 in osteosarcoma cells.

1alpha,25-dihydroxy vitamin D3 has a major role in the regulation of the bone metabolism as it promotes the expression of key bone-related proteins in osteoblastic cells. In recent years it has become increasingly evident that in addition to its well-established genomic actions, 1alpha,25-dihydroxy vitamin D3 induces non-genomic responses by acting through a specific plasma membrane-associated receptor. Results from several groups suggest that the classical nuclear 1alpha,25-dihydroxy vitamin D3 receptor (VDR) is also responsible for these non-genomic actions of 1alpha,25-dihydroxy vitamin D3. Here, we have used siRNA to suppress the expression of VDR in osteoblastic cells and assessed the role of VDR in the non-genomic response to 1alpha,25-dihydroxy vitamin D3. We report that expression of the classic VDR in osteoblasts is required to generate a rapid 1alpha,25-dihydroxy vitamin D3-mediated increase in the intracellular Ca(2+) concentration, a hallmark of the non-genomic actions of 1alpha,25-dihydroxy vitamin D3 in these cells.

Animals↗
PubMed1986

[Determination of vitamin A in food using high-pressure liquid chromatography. Results of a collaborative study of the Vitamin Analysis Working Group following The LMBG Paragraph 35].

A standard method using HPLC for the quantitative determination of vitamin A in food is described. The test material is saponified with aqueous ethanolic potassion hydroxide, and the vitamin A alcohol liberated is extracted with n-hexane. After concentration of the extract, the residue is dissolved in methanol and the vitamin A content determined, after HPLC separation on a RP-C-18 column, by means of an UV or fluorescence detector. The analytic method had been developed by the working group "Vitamin Analysis" within the frame-work of section 35 LMBG; reproducebility and agreement in results between laboratories were checked in vitamin A enriched milk powder and gruel in a collaborative study in which 13 laboratories participated. The statistical evaluation of the results of the collaborative study has shown sufficient reliability to recommend the method for inclusion in the Official List acc. to section 35 LMBG. The method is applicable for the determination of natural vitamin A and vitamin A ester added to dietetic food.

Chromatography, High Pressure Liquid↗
PubMed2003

Selenium combined with vitamin E and vitamin C restores structural alterations of bones in heparin-induced osteoporosis.

The aim of this study was to investigate the effect of heparin on osteoporosis initiation, and the effect of selenium plus vitamins E and C, and the sole combination of vitamins E and C on the progress of osteoporosis induced by heparin through histologic means. Adult female New Zealand white rabbits were divided into three experimental and three control groups. The experimental rabbits were injected with 1000 IU/kg/day heparin (Liquemine) for 4 weeks. These six groups were administered deionized water (CI and EI), 100 mg/kg/day L-ascorbic acid plus 100 mg/kg/day alpha-tocopherol acetate (CII and EII), and 0.05 mg/kg/day sodium selenite, plus these vitamins orally, with a gastric catheter (CIII and EIII), respectively. At the end of the experimental period, the femurs of the animals were collected and investigated under a light photomicroscope. Heparin caused important alterations in bone, such as an improper lamellar structure and a large uncalcified bone matrix. These findings implied the early phase of osteoporosis induced by heparin use. The combination of vitamins E and C given to the experimental rabbits partially prevented this bone tissue destruction. When sodium selenite was given together with vitamins E and C to the osteoporosis model rabbits, the long bone tissue had almost the same structure as in normal rabbits, for example the development of numerous bone trabeculae. Our results suggest that a combination of sodium selenite with vitamins E and C was more effective than combinations of single vitamins to prevent structural alterations in these model bones.

Animals↗
PubMed2003

Vitamin E supplementation increases circulating vitamin E metabolites tenfold in end-stage renal disease patients.

Vitamin E supplementation could elevate circulating vitamin E metabolites while modulating oxidative and inflammatory status in end-stage renal failure patients undergoing hemodialysis. Plasma concentrations of carboxyethyl-hydroxychromanols (alpha- and gamma-CEHC), ascorbic acid, alpha- and gamma-tocopherols, F2-isoprostanes, and inflammatory biomarkers [tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), ferritin, and C-reactive protein (CRP)] were measured in blood samples obtained from patients (n = 11) before and after dialysis on two occasions prior to, and at 1 and 2 mon of daily vitamin E supplementation (400 IU RRR-alpha-tocopherol). Supplementation nearly doubled plasma alpha-tocopherol concentrations (from 18 +/- 0.5 to 31 +/- 1.7 microM, P < 0.0001), whereas gamma-tocopherol concentrations decreased (from 2.8 +/- 0.3 to 1.7 +/- 0.2 microM, P = 0.001). Serum alpha-CEHC increased 10-fold from 68 +/- 3 to 771 +/- 175 nM (P < 0.0001), and gamma-CEHC increased from 837 +/- 164 to 1136 +/- 230 nM (P = 0.008). Vitamin E supplementation also increased postdialysis hematocrits from 38 +/- 1% to 41 +/- 1% (P < 0.001). Dietary antioxidant intakes (vitamins E and C) were low in most subjects; plasma ascorbic acid levels (88 +/- 27 microM) decreased significantly with dialysis (33 +/- 11 microM, P = 0.01). Plasma IL-6, CRP, TNF-alpha, and free F2-isoprostane concentrations were elevated throughout the study. There is a complex relationship between chronic inflammation and oxidative stress that is not mitigated by short-term vitamin E supplementation. Importantly, serum vitamin E metabolite concentrations that increased 10-fold within 30 d of supplementation did not increase further, suggesting routes other than urine for removal of metabolites.

Aged↗
PubMed1981

The cooperative interaction between vitamin E and vitamin C in suppression of peroxidation of membrane phospholipids.

The time course of peroxidation of rat liver microsomes by FeSO4 in the presence of ascorbate showed a delay in the onset of peroxidation compared to the time course when NADPH replaced ascorbate as the electron donor. The delay was consistent with an antioxidant function of ascorbate, possibly mediated through endogenous vitamin E. In order to further investigate the cooperation between ascorbate and vitamin E in suppressing lipid peroxidation, a liposomal system containing polyunsaturated phospholipids was used. Peroxidation was initiated by ferrous iron at pH 5, where spontaneous oxidation of Fe2+ did not occur and the antioxidant properties of ascorbic acid could be characterized independently of its pro-oxidant properties as a reducer of Fe3+. Ascorbic acid alone at concentrations of 30--100 microM delayed peroxidation by 20 min and at higher concentrations prevented peroxidation for 60 min. Physiological levels of vitamin E decreased peroxidation at early time points but the vitamin was apparently consumed during the course of the incubation. The presence of both vitamin C and vitamin E produced suppression of peroxidation at early time points (0--20 min) which was approximately the sum of the individual inhibitions. At longer time points, however, the mixture of antioxidants was much more effective than the sum of both vitamins alone. This suggests that interaction between these antioxidants yields and enhanced delivery of antioxidant protection.

Animals↗