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PubMed1998

Plasma homocysteine, vitamin B6, vitamin B12 and folic acid in end-stage renal disease during low-dose supplementation with folic acid.

In order to see whether conventional low-dose folic acid supplement along with vitamin B6 and B12 reduces hyperhomocysteinemia in patients with ESRD, we compared the levels of homocysteine, vitamin B6, B12 and folic acid among 3 groups of patients: 44 ESRD patients on hemodialysis with replacement of folic acid, vitamin B6, and B12 (dialysis group); 27 chronic renal failure patients without vitamin replacement (predialysis group); and 17 hypertensive patients without vitamin replacement (control group). Mean plasma total homocysteine concentration was higher in the dialysis (15.5 +/- 6.6 micromol/l) and the predialysis groups (15.7 +/- 4.2 micromol/l) than in the control group (6.2 +/- 1.5 micromol/l) (p < 0.001). However, there was no difference in homocysteine concentrations between the dialysis and predialysis groups. In the control and predialysis groups, the homocysteine concentration showed a reverse correlation with the concentrations of folic acid (r = 0.584, p = 0. 014 for the control group; r = 0.431, p = 0.247 for the predialysis group) and vitamin B12 (r = 0.485, p = 0.049 for the control group; r = -0.562, p = 0.023 for the predialysis group) but not with vitamin B6. In conclusion, plasma folic acid concentrations were 3-4 times higher in the dialysis than in the predialysis group. But these levels of folic acid are not enough to reduce hyperhomocysteinemia in ESRD.

Adult↗
PubMed2003

Effect of vitamin E and vitamin C supplementation on antioxidative state and renal glomerular basement membrane thickness in diabetic kidney.

The aim of this study was to analyze the effect of vitamins C and E on malondialdehyde (MDA) content and activities of key antioxidant enzymes: superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) as well as glomerular basement membrane (GBM) thickness in streptozotocin-induced diabetic kidney in rats. Wistar male rats were divided into following groups (12 rats each): the control, diabetic rats, diabetic rats whose drinking water was supplemented with vitamin C in a dose of 1.0 g/l or diet was supplemented with 200 mg of vitamin E/100 g fodder. Body weight, blood glucose and HbA1C levels and 24-hour urinary albumin excretion (UAE) were studied every week (0-12 weeks). After 6 and 12 weeks, MDA content and activities of SOD, CAT and GSH-Px were measured in the kidney homogenate supernatants. Electron micrographs of glomeruli were scanned and morphometric investigations were performed by means of computer image analysis system to compare GBM thickness. The blood glucose and HbA1C concentrations and UAE in diabetic rats were significantly higher than in the control group. An increase in the MDA level and decrease in the SOD, CAT and GSH-Px activities in the kidney of diabetic rats were observed after 6 and 12 weeks of experiment. Administration of vitamins C and E did not affect body weight, blood glucose and HbA1C levels. Both vitamin C and vitamin E decreased lipid peroxidation and augmented the activities of antioxidant enzymes studied in the kidneys of diabetic rats as well as reduced UAE, decreased kidney weight and GBM thickness. The results indicate the potential utility of antioxidant vitamins in the protection against the development of diabetic nephropathy.

Albuminuria↗
PubMed1986

Studies of the vitamin K-dependent carboxylase and vitamin K epoxide reductase in rat liver.

Vitamin K is required as a cofactor for a microsomal enzyme that converts glutamyl residues in precursor proteins to gamma-carboxyglutamyl residues in completed proteins. These residues are essential for the biological function of prothrombin, factors VII, IX, and X, protein C, and protein S. Current data suggest that recognition of protein substrates by the carboxylase requires an unidentified protein-protein interaction in addition to the Glu substrate binding site. The primary vitamin K-dependent event has now been shown to be the abstraction of the gamma-hydrogen of the substrate Glu residue with the concurrent formation of vitamin K 2,3-epoxide. Coumarin anticoagulants appear to inhibit the microsomal vitamin K epoxide reductase and one of a number of microsomal quinone reductases. They therefore block vitamin K action by preventing the recycling of vitamin K epoxide to the quinone and to the active cofactor form, the hydroquinone. Excess vitamin K can reverse a coumarin anticoagulant effect as the nonsensitive quinone reductase can continue to furnish the active coenzyme.

Animals↗
PubMed1988

Effect of vitamin D status on chick kidney proteins: detection of a 45-kilodalton mitochondrial protein suppressed by vitamin D.

Two-dimensional polyacrylamide gel electrophoresis along with L-[35S]methionine radiolabeling studies were used to examine the effect of chronic vitamin D status on the composition and relative abundance of chick kidney proteins. Comparison of silver-stained gels revealed no extensive differences in either the electrophoretic mobility or the amounts of kidney proteins present in the mitochondrial fraction from vitamin D-replete and vitamin D-deficient chicks. A similar result was obtained in studies with L-[35S]methionine-labeled proteins. Vitamin D deficiency specifically elevated levels of a 45-kilodalton mitochondrial protein (pI 5.0 to 5.5) by approximately 5- to 12-fold relative to amounts present in vitamin D-replete tissue. This protein could not be detected in postmitochondrial supernatant fractions and was only faintly visible in crude kidney homogenates. The specificity of the observed suppression of this 45-kilodalton protein by vitamin D suggests that it may play an important role in renal functions influenced by the vitamin D endocrine system.

Animals↗
PubMed1997

"Vitamin CE," a novel prodrug form of vitamin E.

Reaction of 5a-bromo-alpha-tocopherol with ascorbic acid produces 5a-tocopheryl ascorbate which is designated "vitamin CE." This novel tocopherol derivative represents an interesting prodrug form of alpha-tocopherol (vitamin E) that is stable under acidic conditions, but regenerates finely dispersed vitamin E in basic media. The reaction mechanism of the base-induced decomposition of vitamin CE involves elimination of ascorbate and production of an ortho-quinone methide intermediate that oxidizes ascorbate, and is reduced to vitamin E. Kinetic experiments showed reaction to proceed in the pH range of 8 to 11 under physiological conditions. Tissue culture measurements demonstrated that vitamin E generated from the novel derivative is absorbed at much higher rates than conventional preparations and can even be absorbed under simulated conditions of malabsorption where there is no uptake of conventional vitamin E medications.

Absorption↗
PubMed2005

Nonradioactive vitamin B12 absorption test evaluated in controls and in patients with inherited malabsorption of vitamin B12.

BACKGROUND: Current tests for evaluation of vitamin B(12) absorption are problematic because they involve the use of radioactively labeled vitamin B(12). We describe a vitamin B(12) absorption test that circumvents this problem. METHODS: We measured cobalamin or transcobalamin saturated with cobalamin (holo-TC) 24 h after three 9-microg doses of vitamin B(12) given orally at 6-h intervals. We studied 17 patients with inherited malabsorption of vitamin B(12) attributable to Imerslund-Grasbeck syndrome (n = 13) or intrinsic factor deficiency (n = 4), their obligate heterozygous biological parents (n = 19), and healthy controls (n = 44). RESULTS: In the patients, the median (range) change of holo-TC after the B(12) load was not significant [1 (-42 to 5) pmol/L], nor was the change of cobalamin [-3 (-32 to 22) pmol/L], consistent with a lack of measurable active or passive absorption. In controls, however, the median (range) increases of holo-TC and cobalamin were 26 (-6 to 63) pmol/L and 41 (-37 to 109) pmol/L, respectively. Similarly, the parents showed increases of 23 (-2 to 47) pmol/L and 27 (-15 to 94) pmol/L. The mean areas under the ROC curves (95% confidence intervals) were 0.97 (0.93-1.0) for holo-TC and 0.87 (0.79-0.94) for cobalamin, distinguishing patients from controls. At a cutoff of 6 pmol/L for holo-TC, the diagnostic sensitivity (95% confidence interval) was 100 (81-100)%, and the diagnostic specificity was 92 (82-97)%. CONCLUSION: Measurement of holo-TC after administration of vitamin B(12) is a promising approach for evaluating vitamin B(12) absorption.

Absorption↗
PubMed1997

Improving the vitamin K status of breastfeeding infants with maternal vitamin K supplements.

OBJECTIVE: To increase the phylloquinone (vitamin K1) concentration of human milk with maternal oral phylloquinone supplements such that both the phylloquinone intake of breastfed infants and their serum concentrations of phylloquinone would approach those of formula-fed infants who are known to be at much less risk for hemorrhagic disease of the newborn. DESIGN: Two stages: stage I, longitudinal, randomized study of 6 weeks' duration; and stage II, longitudinal, randomized, double-blind, placebo-controlled study of 12 weeks' duration. SETTING: Patients from a private pediatric practice in Madison, WI. PATIENTS: Stage I: sequential sampling of 20 lactating mothers to determine the level of maternal supplementation needed in stage II. Ten mothers received 2.5 mg/d oral phylloquinone, and 10 mothers received 5.0 mg/d oral phylloquinone. Stage II: sequential sampling of 22 human milk-fed infants and lactating mothers. All infants received 1 mg of phylloquinone at birth. Eleven mothers received a placebo; 11 mothers received 5 mg/d phylloquinone. MEASUREMENTS AND RESULTS: In stage I, both 2.5 and 5.0 mg/d phylloquinone significantly increased the phylloquinone content of human milk at both 2 and 6 weeks. As expected, 5.0 mg had a greater effect (mean +/- SD, 58.96 +/- 25.39 vs 27.12 +/- 12.18 ng/mL at 2 weeks). In stage II, the vitamin K-supplemented group had significantly higher maternal serum phylloquinone concentrations, higher phylloquinone milk concentrations, and higher infant plasma phylloquinone concentrations at 2, 6, and 12 weeks compared with the placebo group. At 12 weeks infant phylloquinone intakes were significantly higher for the vitamin K group than the placebo group (9.37 +/- 4.55 vs 0.15 +/- 0.07 microgram/kg per day). This corresponded to a plasma phylloquinone concentration in the vitamin K group of 2.84 +/- 3.09 vs 0.34 +/- 0.57 ng/mL in the placebo group. At 12 weeks, the prothrombin times did not differ between the groups, but the des-gamma-carboxy-prothrombin (partially carboxylated prothrombin thought to be a measure of vitamin K deficiency) was significantly elevated in the placebo group compared with the vitamin K group (1.48 +/- 1.19 vs 0.42 +/- 0.55 ng/mL). CONCLUSION: In exclusively breastfed infants who receive intramuscular phylloquinone at birth, the vitamin K status as measured by plasma phylloquinone and des-gamma-carboxy-prothrombin concentrations is improved by maternal oral supplements of 5 mg/d phylloquinone through the first 12 weeks of life.

Food, Fortified↗
PubMed1986

Relationship between the vitamin D content of maternal milk and the vitamin D status of nursing women and breast-fed infants.

This work was designed to study the effect of the vitamin D content of human milk on the vitamin D status of exclusively breast-fed infants, and the relation between milk and maternal serum concentrations of vitamin D during the first month of lactation. Serum levels of calcium (Ca), phosphorus (P), magnesium (Mg) and 25-hydroxyvitamin D (25-OH-D) were determined in a racially heterogeneous population of nursing women, between days 3 and 5 (L3), 15 and 18 (L15) and 30 and 45 (L30) post partum. The same parameters were determined in the serum of 1-month-old breast-fed infants. Maternal milk samples were obtained at L3, L15 and L30 and analysed for Ca, P, Mg, vitamin D and 25-OH-D content. Milk levels of Ca, P and Mg were found to be within the range previously described by other authors. No correlation was found between serum and milk levels of vitamin D and 25-OH-D in nursing mothers. The 25-OH-D concentration in milk was related to its vitamin D content and strongly correlated (P less than 0.001) with the 25-OH-D levels in the serum of exclusively breast-fed infants. No significant changes were observed in maternal serum levels of 1,25-dihydroxyvitamin D (1,25-(OH)2D3) measured at L3 and L30, or between maternal and infant levels of 1,25-(OH)2D3 at L30. This study emphasizes the importance of the 25-OH-D content of maternal milk, in being primarily responsible for the vitamin D concentrations found in the serum of exclusively breast-fed infants.(ABSTRACT TRUNCATED AT 250 WORDS)

Breast Feeding↗
PubMed1989

Vitamin K-reversible hypoprothrombinemia in rats: comparison of hypoprothrombinemic changes in various strains of rats caused by vitamin K deficiency and antibiotic treatment.

Hypoprothrombinemic changes were compared in rats fed various vitamin K-deficient diets. Changes such as prolongation of prothrombin time and activated partial thromboplastin time, decrease in plasma levels of prothrombin and clotting factor VII, and increase in plasma descarboxyprothrombin, appeared in rats maintained on vitamin K-deficient diet, but in rats on ordinary diet (vitamin K-sufficient diet). As the development of hypoprothrombinemia was not significantly different among animals fed various vitamin K-deficient diets, the blood coagulation parameters were concluded to be regulated only by the vitamin K level. Following the development of hypoprothrombinemia, hemorrhaging in various organs was detected in vitamin K-deficient rats, with strain differences in the severity of hemorrhage; Fischer and Wistar strains were more sensitive than the Sprague Dawley strain. Administration of a beta-lactam antibiotic, latamoxef (LMOX), to vitamin K-deficient rats led to enhancement of the hypoprothrombinemic conditions, but LMOX-associated changes in plasma enzyme levels were not detected.

Animals↗
PubMed1978

Nutritional vitamin-B12 deficiency. Possible contributory role of subtle vitamin-B12 malabsorption.

Dietary deficiency of vitamin B-12 has been reported, yet most people ingesting vitamin-B12-deficient diets even for many years appear to achieve a balance that does not lead to overt signs and symptoms of deficiency. I present the case of a vegan of 25 years' duration who developed severe neurologic abnormalities due to vitamin-B12 deficiency. His diet provided 1.2 microgram of vitamin B12 daily at most. Despite normal Schilling test findings, he absorbed subnormal amounts of vitamin B12 given with ovalbumin. This poor absorption appeared to be related to his gastritis, achlorhydria, and subnormal intrinsic-factor secretion. Probably, vitamin-B12 deficiency in this patient resulted from both dietary restriction and the subtle malabsorption, neither of which would have sufficed alone to produce the clinical problem. Possibly such malabsorption may also be present in many of those vegans developing overt vitamin-B12 deficiency in whom Schilling test findings have been normal.

Diet, Vegetarian↗
PubMed2000

[Effects of vitamin E and vitamin C on nonenzymatic glycation and peroxidation in experimental diabetic rats].

SD rats were peritoneally injected with streptozotocin (STZ) to establish diabetic animal model. The changes of nonenzymatic glycation and peroxidation in rats supplemented with vitamin C and/or vitamin E during five weeks were investigated. It was found that the glycated hemoglobin, glycated LDL, renal cortical AGEs and MDA in sera and renal cortex significantly decreased after supplementation of vitamins E and C jointly. It was also observed that the MDA in serum and the cortex of kidney but not glycated hemoglobin, glycated LDL and AGEs significantly decreased in the groups supplemented with vitamin C or vitamin E separately. The results suggested that joint supplementation of vitamin C and vitamin E could inhibit nonenzymatic glycation obviously and peroxidation in diabetic rats and protect the kidney from damage under hyperglycemia.

Animals↗
PubMed2004

Lipid peroxidation in relation to vitamin C and vitamin E levels.

Oxidative stress plays an important contributory role in the pathogenesis of age-related chronic diseases. Increased lipid peroxidation process is caused by an enhanced free radical formation together with a higher supply of substrates and by an insufficient defense by antioxidants as well. Levels of malondialdehyde to content of lipid peroxidation substrates (polyunsaturated fatty acids), promoters (homocysteine--hydroxyl radical producer) and inhibitors (essential vitamins C and E) were estimated in a group (n=92) of subjective healthy adults randomly selected from general population. The relationship of malondialdehyde levels to values of peroxidisability index of fatty acids as well as to levels of homocysteine is significantly positive linear A significant inverse linear correlation between malondialdehyde levels and natural antioxidant levels (vitamin C, vitamin E) was recorded. Lipid peroxidation products (conjugated dienes of fatty acids--initial, malondialdehyde--secondary) are significantly increased in groups of subjects with deficient levels of vitamin C (below the limit from antioxidative point of view), vitamin E and both vitamins, if compared to group with normal vitamin levels (over limit in accordance with antioxidative criterion). The results document that the deficiency in two key antioxidants for lipid peroxidation inhibition means the insufficient defense against free radicals and the increased lipid peroxidation.

Adult↗
PubMedDate not supplied

Is 1,25-dihydroxyvitamin D3 the specific vitamin D3 metabolite active on insulin release and calcium handling by islets from vitamin D3-deprived rats?

Vitamin D3 treatment can improve within 3 days the low insulin secretion of vitamin D3-deficient rats. One of its metabolite active in vivo, 1,25(OH)2D3 cannot stimulate the insulin secretion in vitro within 2 h, except when islets came from 24 h-vitamin D3 prepared rats. These findings led us to determine the respective in vitro activity of three vitamin D3 metabolites [1,25(OH)2D3; 24,25(OH)2D3 and 25(OH)D3] on cellular events in perifused islets derived from vitamin D3-deficient rats which were injected with vitamin D3 24 h earlier. Three experimental conditions were studied: either a rise in metabolite concentration during a steady-state 8.3 mmol/l glucose medium, or without glucose, or a rise in glucose concentration (16.7 mmol/l) during a steady-state vitamin D3 metabolite concentration. The 1,25(OH)2D3 was the only of the 3 metabolites active both on insulin release and 45Ca2+ efflux. None of the three metabolites modified K+ fluxes (86Rb as a tracer). The in vitro specific stimulatory action of 1,25(OH)2D3 on B cell was rapidly seen within a few minutes, and occurred only in the presence of glucose stimulation. These results suggest that 1,25(OH)2D3 might potentiate the insulin response to glucose by an action on Ca2+ handling, either by enhancing Ca2+ entry in the B cell and/or Ca2+ mobilization from intracellular organelles.

Animals↗
PubMed2006

[The influence of the vitamin-mineral complex upon the blood vitamin, calcium and phosphorus of patients with ostreoarthrosis].

In research in which 11 osteoarthrosis patients with osteoarthrosis of the knee-joint of II-III degree and 18 healthy people took part, it has been shown that sufficiency with vitamin C, carotinoids and calcium of osteoarthrosis patients was worse than that of healthy people. These micronutrients blood plasma level in both groups was less than the lower border of normal sufficiency. Whereas patients from both groups were adequately supplied with vitamins A, E, B2 and phosphorus. Addition of vitamin-mineral complex to patients ration course 30 days resulted in eliminating insufficiently of vitamin C, carotinoids, beta-carotin, calcium and in hardly noticable changes of initial high levels of vitamin A, E, B and phosphoris. These nutrients deficit disappeared while there was no noticeable change in the initial optimal provision with vitamins B2, A and E. Thus, there is no doubt in arguments in favour of additional enrichment with vitamins and calcium of osteoarthrosis patients diet.

Adult↗
PubMed1989

Vitamin D requirements and vitamin D intoxication in infancy.

Without vitamin D supplementation, the majority of infants seems to be at risk of vitamin D-deficiency rickets. On the other hand, routine vitamin D supplementation of breast-fed infants is not recommended by all authors. In this paper we give an overview of vitamin D metabolism and vitamin D regulation in newborns, which may differ in a certain way from the regulation in adults. Based on this, minimal and optimal requirements for vitamin D in newborns and infants is determined. Furthermore, the paper aims at defining dosages and conditions that are at risk of vitamin D intoxication.

Humans↗
PubMed1988

Vitamin status of inpatients with chronic cephalgia and dysfunction pain syndrome and effects of a vitamin supplementation.

66 female inpatients with dysfunction pain syndrome, chronic cephalgia and facial pain participated in a randomized, placebo-controlled double-blind study, half the patients receiving a multivitamin preparation for 12 days and the other half a placebo. The biochemically determined vitamin status at the start of the study revealed gaps in the coverage of the vitamin supply, particularly with regard to the vitamins thiamin, riboflavin and folic acid. 65% of the patients showed a subclinical vitamin deficiency of two or more vitamins. With regard to the development of pain during the study no statistically significant differences could be determined, however, between the active-treatment and placebo groups. Nevertheless, a clear reduction in pain was more frequently observed in the active-treatment group, and a deterioration of pain more frequently in the placebo group. A reduction in pain was reported more often by patients in whom the values of alpha-ETK, alpha-EGOT, folic acid and cyanocobalamin improved in the course of the study. Vitamin administration in physiological doses evidently have only weak effects on the behavior of pain; analgesic vitamin effects may be presumed in the case of correspondingly high therapeutic doses for a prolonged period.

Adult↗
PubMed1988

Vitamin D-deficiency in the elderly: treatment with ergocalciferol and hydroxylated analogues of vitamin D3.

The purpose of the present work was to study the effect of vitamin D and its metabolites in correcting hypovitaminosis D in the elderly. Thirty elderly people (mean age 78.4 years) participated in this study. They all had low serum levels of 25-hydroxyvitamin D (25-OH-D), of 24,25-dihydroxyvitamin D [24,25(OH)2D] and of 1,25-dihydroxyvitamin D [1,25(OH)2D]. These low levels did not increase in nine subjects after oral administration of vitamin D2 (3,000 IU/day for 12 weeks). However, administration of 1 alpha-hydroxyvitamin D3 (1 alpha-OH-D3) to 12 other subjects (0.5 micrograms/day for 8 weeks) led to a significant increase in the serum levels of 1,25(OH)2D. The other vitamin D metabolite levels remained unchanged. A significant increase in the levels of all three main vitamin D metabolites was obtained following administration of 25-hydroxyvitamin D3 (25-OH-D3) to a third group of nine subjects (25 micrograms/day for 1 week). These results suggest that vitamin D nutrition in elderly people insufficently exposed to the sun could be maintained by regular administration of 25-OH-D, whereas the administration of native vitamin D (ergocalciferol) in the doses used was inadequate for vitamin D nutrition.

24,25-Dihydroxyvitamin D 3↗
PubMed1995

Comparison of two levels of vitamin C supplementation on antioxidant vitamin status in elderly institutionalized subjects.

The concentrations of antioxidant vitamins, particularly vitamin C, are often low in the plasma of institutionalized elderly subjects, and could explain their susceptibility to oxidative stress. However, as such low levels were not always found in home-living healthy elderly persons, the antioxidant vitamin depletion in the formers could result from environmental conditions better than aging itself. The objective of this study was therefore to verify the antioxidant vitamin status in institutionalized elderly persons and to evaluate if a low vit C supplement could be sufficient to improve the plasma vit C concentration in those subjects. This study confirms that plasma vitamin C levels are in the scurvy range in 20 elderly institutionalized subjects and significantly lower than in healthy home-living elderly persons. Beta-carotene concentrations were found marginally low but alpha-tocopherol levels were in the normal range. All three vitamins were correlated. Fifteen days on a physiological vitamin C (150 mg/day) supplementation was sufficient to restore normal vit C levels (50 mumol/l). A further pharmacological vit C administration (750 mg/day) during 30 days only allowed a marginal increase in the plasma vit C concentrations.

Aged↗