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PubMed2006

Bioavailability of vitamins A and E from whole and vitamin-fortified milks in control subjects.

BACKGROUND: Dairy products fortified with vitamins and minerals represent a growing market that is of interest to those sectors of the population with unbalanced diets and increased needs. However, there is little information on the bioavailability of micronutrients in milk products at dietary intake levels. AIM OF THE STUDY: To evaluate the bioavailability of vitamins A and E in whole milk and fortified whole and skimmed milk in control subjects. METHODS: A single-dose bioavailability study was performed using three commercially available milks (unfortified whole milk and whole and skimmed milk fortified with vitamins A and E). Nineteen volunteers (10 women and 9 men) ingested 430 ml of each milk on different days. The contents of retinol and alpha-tocopherol provided in the milks and the retinyl esters and alpha-tocopherol in triglyceride-rich lipoprotein fractions (TRL) from plasma collected for 6.5 h postprandially were assayed using a quality-controlled HPLC method. The relative absorption of vitamins A and E from milks was calculated on the basis of area under the curve (AUC) versus time curve estimations, adjusted for plasma volume and expressed as percentage of the amount of nutrient provided. RESULTS: The total amounts of retinol and alpha-tocopherol provided ranged between 0.48 and 4.15 micromol and 0.41 and 32.49 micromol, respectively. The AUC value of retinyl palmitate in TRL was higher for fortified whole milk than for the other two milks (unfortified whole and fortified skimmed milk). The percent relative absorption of vitamin A did not differ among the three types of milk. The AUC for alpha-tocopherol was no different after the ingestion of any of these milks. CONCLUSION: The mean percentage of retinol absorption was apparently similar for the three types of milk, regardless of the amount of fat ingested with each type of milk and the vitamin A provided.

Adult↗
PubMed2006

Disulfide-dependent protein folding is linked to operation of the vitamin K cycle in the endoplasmic reticulum. A protein disulfide isomerase-VKORC1 redox enzyme complex appears to be responsible for vitamin K1 2,3-epoxide reduction.

Gamma-carboxylation of vitamin K-dependent proteins is dependent on formation of reduced vitamin K1 (Vit.K1H2) in the endoplasmic reticulum (ER), where it works as an essential cofactor for gamma-carboxylase in post-translational gamma-carboxylation of vitamin K-dependent proteins. Vit.K1H2 is produced by the warfarin-sensitive enzyme vitamin K 2,3-epoxide reductase (VKOR) of the vitamin K cycle that has been shown to harbor a thioredoxin-like CXXC center involved in reduction of vitamin K1 2,3-epoxide (Vit.K>O). However, the cellular system providing electrons to the center is unknown. Here data are presented that demonstrate that reduction is linked to dithiol-dependent oxidative folding of proteins in the ER by protein disulfide isomerase (PDI). Oxidative folding of reduced RNase is shown to trigger reduction of Vit.K>O and gamma-carboxylation of the synthetic gamma-carboxylase peptide substrate FLEEL. In liver microsomes, reduced RNase-triggered gamma-carboxylation is inhibited by the PDI inhibitor bacitracin and also by small interfering RNA silencing of PDI in HEK 293 cells. Immunoprecipitation and two-dimensional SDS-PAGE of microsomal membrane proteins demonstrate the existence of a VKOR enzyme complex where PDI and VKORC1 appear to be tightly associated subunits. We propose that the PDI subunit of the complex provides electrons for reduction of the thioredoxin-like CXXC center in VKORC1. We can conclude that the energy required for gamma-carboxylation of proteins is provided by dithiol-dependent oxidative protein folding in the ER and thus is linked to de novo protein synthesis.

Animals↗
PubMed2006

Dietary intake of vitamin B6 and concentration of vitamin B6 in blood samples of German vegans.

OBJECTIVE: The study aimed to evaluate the dietary vitamin B6 intake and determine the vitamin B6 concentration in blood samples of German vegans. DESIGN AND SETTING: Cross-sectional study with 33 examination sites all over Germany. Subjects Ninety-three vegans (50 females) with a mean (+/- standard deviation (SD)) age of 43.7 +/- 15.7 years who took no vitamin supplements. METHODS: Dietary intake was assed using a semi-quantitative food-frequency questionnaire. Erythrocyte aspartate aminotransferase activity coefficient (EAST-AC) was calculated as the ratio of stimulated (pyridoxal 5'-phosphate added) to unstimulated activity in blood samples that were provided after an overnight fast. RESULTS: Mean +/- SD vitamin B6 intake was 2.83 +/- 0.98 mg day(-1) and mean +/- SD protein intake was 56.6 +/- 21.7 g day(-1). Of the participants 4% showed vitamin B6 intakes lower than daily recommended intakes for Germany, 16% showed EAST-AC > 1.85, and a further 58% showed EAST-AC of 1.5-1-85. Moderate vegans were affected to a lesser extent than strict vegans. None of the established confounders was a significant predictor of EAST-AC. In logistic regression analyses the contribution of nutriments and cereals to pyridoxine intake was the only predictor of EAST-AC classified as < or = 1.85 and > 1.85, respectively. CONCLUSIONS: In spite of the high total intake of vitamin B6, an adequate concentration in blood samples could not be realised for a majority of the participants. Due to the health implications of a marginal pyridoxine status, vegans should be encouraged to include foods with a high bioavailability of pyridoxine, such as beans, lentils and bananas, in the daily diet.

Adult↗
PubMed1997

Olestra's effect on vitamins D and E in humans can be offset by increasing dietary levels of these vitamins.

One hundred two normal healthy males and females were given 0, 8, 20 or 32 g/d olestra to which had been added graded amounts of vitamins A, D and E for 8 wk in a parallel, double-blind study. The primary purpose of the study was to determine the amounts of vitamins D and E needed to offset the effect of olestra on the availability of these vitamins. Serum concentrations of retinol, carotenoids, 25-hydroxyvitamin D metabolites, alpha-tocopherol, phylloquinone, lipids, ferritin and total iron, iron-binding capacity and hematology parameters, plasma concentrations of des-gamma-carboxyprothrombin and prothrombin, and urinary gamma-carboxyglutamic acid (Gla) excretion were measured biweekly. Clinical chemistry and urinalysis parameters, vitamin B12 absorption, and serum 1,25-dihydroxyvitamin D concentration were measured at wk 0 and 8. Serum concentrations of alpha-tocopherol and 25-hydroxyergocalciferol were restored to control concentration by adding 2.1 mg d-alpha-tocopheryl acetate and 0.06 microg ergocalciferol per gram of olestra, respectively, to the diet. Olestra reduced serum concentrations of 25-hydroxyergocalciferol, carotenoids and phylloquinone in a dose-responsive manner but did not affect Gla excretion, plasma des-gamma-carboxyprothrombin and prothrombin concentrations, overall vitamin D status, vitamin B12 absorption or iron status. Laboratory evaluations showed no olestra-related effects. Subjects in all groups reported mild to moderately severe transient gastrointestinal symptoms. These symptoms did not affect study compliance or the integrity of the data.

25-Hydroxyvitamin D 2↗
PubMed1992

Vitamin K prophylaxis and vitamin K deficiency bleeding (VKDB) in early infancy.

The efficacy of vitamin K prophylaxis (1 mg im or sc, or 1-2 mg orally both given as a single dose at birth) in the prevention of vitamin K deficiency bleeding in early infancy was estimated in Germany during a 15-month period between 1988 and 1989. Cases were identified by a survey of all paediatric hospitals and population denominators by a survey of all obstetric hospitals. Response rates were 85% and 68%, respectively. Thirteen cases of vitamin K deficiency bleeding in early infancy with confirmed prophylactic states were confirmed, seven of whom had intracranial haemorrhage. The estimated efficacy of single parenteral administration of vitamin K versus no prophylaxis was 96.7% (95% confidence interval: 74-99.6%) and for single oral administration versus no prophylaxis 80.4% (9.1-95.6%). Single parenteral vitamin K prophylaxis gave substantial protection against vitamin K deficiency bleeding in early infancy. Single oral prophylaxis appeared to be less effective, although the difference was not significant, as indicated by the wide overlap of the respective 95% confidence intervals.

Administration, Oral↗
PubMed1969

Vitamin K and coumarin anticoagulants: dependence of anticoagulant effect on inhibition of vitamin K transport.

Coumarin anticoagulants inhibit the release of plasma clotting factor VII by vitamin K in liver slices from vitamin K-deficient animals without inhibition of protein synthesis. When the ratio of vitamin K to coumarin anticoagulant is kept constant, but the concentrations are increased, the inhibition disappears. This suggests that the pharmacological action of coumarin anticoagulants depends on irreversible inhibition of normal vitamin K transport to its site of action. At higher concentrations of vitamin K the inhibition can be surmounted, because vitamin K can enter the cell by an alternate route that is not inhibited by coumarin anticoagulants.

Animals↗
PubMed1999

Modulation of fat-soluble vitamin concentrations and blood mononuclear leukocyte populations in milk replacer-fed calves by dietary vitamin A and beta-carotene.

Dairy calves (n = 18), separated from dams at birth, were fed 1 L of pooled-colostrum. For the remaining 7 wk of the study, they were fed one of three diets consisting of either a custom-formulated milk replacer without vitamin A (controls), or supplemented with retinyl palmitate (equivalent to 32,000 IU of vitamin A/d) or with beta-carotene (equivalent to 20,000 IU of vitamin A/d). Plasma retinol, beta-carotene, and RRR-alpha-tocopherol concentrations were lowest at birth, and increased substantially from birth to 1 wk postpartum in all groups, a probable consequence of ingestion of colostrum. From 1 to 7 wk of age, retinol concentrations were greatest in retinyl palmitate-supplemented calves, intermediate in beta-carotene-supplemented calves and lowest in control calves. At 2, 3, 5, 6, and 7 wk, RRR-alpha-tocopherol concentrations were lower in retinyl palmitate-supplemented calves than in control calves. A negative correlation between plasma retinol and vitamin E concentrations existed from wk 2 to 7, suggesting vitamin A influences the absorption and distribution of RRR-alpha-tocopherol. Supplemental retinyl palmitate, but not beta-carotene, was associated with a reduction in the percentage of blood mononuclear leukocytes expressing CD2, CD4, and CD8-T cell antigens and interleukin-2 receptors. By wk 7, leukocyte populations from retinyl palmitate-supplemented calves were more similar to those from adult cattle than those from control calves, suggesting that supplemental vitamin A, as retinyl palmitate, affects the maturation of the neonatal immune system. Differences in the composition of blood mononuclear leukocyte populations may represent changes in immune competency.

Animals↗
PubMed1994

The contribution of vitamin K2 (menaquinones) produced by the intestinal microflora to human nutritional requirements for vitamin K.

BACKGROUND: Coagulopathy manifest by elevation of the prothrombin time (PT) in patients receiving broad spectrum antimicrobials indirectly suggests a role for intestinal microflora synthesized menaquinone (MK) in the maintenance of normal coagulation. Nonetheless, no direct evidence is available to support this contention. OBJECTIVE: Our objective was therefore to provide evidence that bacterially produced MK may be absorbed by the distal small bowel of humans. METHODS: Using a cell harvester, Staphylococcus aureus (ATCC 29213) was grown in 12-L batches, harvested, and extracted by high performance liquid chromatography (HPLC) to obtain 8 mg of pure MK. Four normal volunteers were placed on a diet severely restricted in vitamin K1 (median 32-40 U/day), and were given warfarin to maintain an International Normalized Ratio of approximately 2.0. On the 10th day of warfarin administration, naso-ileal intubation was performed and 1.5 mg of MK was delivered into the ileum. PT, factor VII, II and serum vitamin K1 levels were monitored throughout the study. RESULTS: Mean serum vitamin K1 levels were reduced to 30% of the pre-diet value at the time of MK administration. Within 24 h of ileal MK administration, there was a significant (p < 0.05) increase in the factor VII level of 0.28 +/- 0.10 U/ml (mean +/- SEM) and a significant decrease of 2.5 (+/- 0.1) s in the PT, whereas in the control phase (during which no MK was administered), there were no significant changes in the PT or factor VII at corresponding time intervals. CONCLUSION: These data provide direct evidence for the absorption of vitamin K2 from the distal small bowel, supporting a definite role for bacterially synthesized vitamin K2 in contributing to the human nutritional requirements of this vitamin.

Adult↗
PubMed1999

Proposed standard for human blood vitamin B1 value using HPLC. The Committee for Vitamin Laboratory Standards, Japan.

Standard reference ranges for all laboratory test values are mandatory. This study was designed to establish a reference range for blood vitamin B1 levels, since the normal range has not been determined in the Japanese population. We founded the Japan Committee for Vitamin Laboratory Standards, which was incorporated with the Vitamin Society of Japan and the Japanese Society of Nutrition and Food Science. We standardized whole blood vitamin B1 levels using three HPLC techniques (post-column reverse-phase HPLC, pre-column reverse-phase HPLC, and precolumn GP-HPLC). The reference range was obtained in 54 volunteers administered a 1,800 kcal diet with 2 mg of vitamin B1 (1.74 mg measured) daily to avoid marginal vitamin B1 deficiency in the population. The range for each assay was 26-47, 28-51, and 28-56 ng/ml, respectively. Our data suggest that 26-28 ng/ml is the lower limit of normal for whole blood vitamin B1, but further studies in a larger population are needed in order to obtain more definitive results.

Chromatography, High Pressure Liquid↗
PubMed1978

Vitamins in intravenous feeding: a study of water-soluble vitamins and folate in critically ill patients receiving intravenous nutrition.

Red cell B vitamins, folate and white cell vitamin C were measured in a group of critically ill surgical patients before and following a course of intravenous nutrition. Patients received a widely used vitamin supplementation regimen in the form of one ampoule of water-soluble vitamins daily and recommended doses of intramuscular folate, vitamin B12 and vitamin K weekly. This regimen was adequate to maintain tissue levels of the water-soluble vitamins and folate. Patients with initially low values had normal values at the end of the treatment period.

Ascorbic Acid↗
PubMed1986

Vitamin D-dependent rickets type II: extreme end organ resistance to 1,25-dihydroxy vitamin D3 in a patient without alopecia.

Vitamin D-dependent rickets type II (VDDR II) is a rare syndrome resulting in severe rickets and is resistant to treatment with vitamin D and its derivatives. Patient with this disease, who are frequently the children of consanguinous marriages, present with elevated circulating concentrations of 1,25-dihydroxy vitamin D, the active metabolite of vitamin D, and in vitro studies have indicated a failure of intracellular binding of the hormone. Alopecia has been noted in many of these patients and it has been suggested that this feature may indicate a more marked resistance to treatment. However we describe a 3-year-old boy with this disease who, although having normal hair growth, displayed extreme resistance to treatment with active vitamin D metabolites. In vitro studies of skin fibroblasts disclosed not only an absence of hormone binding or 1,25(OH)2D3-induced 24-hydroxylase activity but reduced metabolism of 1,25(OH)2D3 itself. In this child, treatment with exogenous 1,25-dihydroxy vitamin D3 at doses of up to 24 micrograms/day, which increased the circulating concentration of the metabolite to greater than 100 times the normal adult mean, failed to alleviate his condition and he died at the age of 39 months. This would therefore suggest that absence of alopecia, in this condition, cannot be regarded as a constant predictive sign of a lesser resistance and of responsiveness to Vitamin D treatment.

Calcitriol↗
PubMed1995

Potent vitamin D3 analogs: their abilities to enhance transactivation and to bind to the vitamin D3 response element.

1,25 dihydroxyvitamin D3 [1,25(OH)2D3] mediates its biological activities through specific binding to the vitamin D3 receptor (VDR) and subsequent association with vitamin D3 responsive elements (VDRE) in genes modulated by 1,25(OH)2D3. Several novel vitamin D3 compounds (Cmpds) have recently been identified which have 5- to 1000-fold greater abilities to induce differentiation and to inhibit proliferation of HL-60 leukemic blast cells as compared to the parental 1,25(OH)2D3 (code name, Cmpd C). To clarify the mechanism by which five of these vitamin D3 analogs [1,25(OH)2-16ene-D3, (Cmpd HM); 1,25(OH)2-16ene-23yne-D3, (Cmpd V); 1,25(OH)2-16ene-23yne-26,27 F6-D3; 22-Oxa-1,25(OH)2D3; 1,25(OH)2-23yne-D3] mediate their remarkably potent biological activities, we have investigated their abilities in HL-60 cells to transactivate a chloramphenicol acetyl transferase (CAT) reporter gene containing a VDRE from the human osteocalcin gene attached to a thymidine kinase minimal promoter. Also, the abilities of the analogs to enhance the binding of the human recombinant VDR/retinoic X receptor alpha (RXR alpha) heterodimer to the VDRE were examined in gel mobility shift assays. In serumless cultures, a series of potent vitamin D3 analogs had comparable abilities to transactivate the reporter gene as did the biologically less potent 1,25(OH)2D3 (approximately 15-20-fold stimulation in cultures containing 2 x 10(-8)M of vitamin D3 cmpds). Biologically very weak inducers of differentiation of HL-60 [24R,25(OH)2D3; 25(OH)-16ene-23yne-D3] had markedly diminished abilities to induce transactivation. Dose-response studies of Cmpds C, V, HM (10(-7)-10(-11)M) showed that in serumless culture conditions, transactivation of the VDRE-CAT was similar; however, in the presence of serum, Cmpd C at 10(-9)M had 20-fold less activity than analogs V and HM. These results may reflect increased binding of Cmpd C to the D binding protein (DBP) in serum as compared to the lower binding affinities for DBP by Cmpds HM and V. Affinities of the biologically potent analogs for VDR did not parallel their abilities either to transactivate VDRE-CAT or to mediate a biological affect on HL-60 cells. In further studies, gel mobility shift assays showed that VDR alone did not have detectable binding to VDRE; likewise, VDR plus RXR had little binding to VDRE in the absence of ligand. In contrast, biologically active vitamin D3 compounds (Cmpds HM, C, V) in a dose-dependent fashion enhanced the VDR/RXR (retinoid X receptor)-VDRE retarded band.(ABSTRACT TRUNCATED AT 400 WORDS)

Base Sequence↗
PubMed2004

Effects of pharmacological doses of Vitamin D3 on mineral balance and profiles of plasma Vitamin D3 metabolites in horses.

Metabolism and functions of Vitamin D in horses differ from those in humans, pigs and rats. In horses, calcidiol and calcitriol concentrations in blood plasma are remarkably low (<10 nmol L(-1); 20-40 pmol L(-1), respectively). When a toxic amount of Vitamin D(3) is administered, the responsiveness of calcium and calcitriol concentrations in blood plasma is much reduced compared to the other domestic animal species but inorganic phosphate (Pi) response is much more marked, leading to an increase of the Ca x Pi product. Also, soft tissue calcifications have been observed to develop in horses during Vitamin D(3) intoxication. It was suggested that the elevation of the Ca x Pi product may play a causative role in this calcification process. To test this assumption, two horses were treated with 40,000 IU kg(-1) of Vitamin D(3) whilst dietary uptake of Ca and Pi was restricted to prevent or to diminish the increase of the Ca x Pi product. Distribution, number and severity of calcification centres were considerably less in these horses than in the control animals of a previous experiment which had received the same amount of Vitamin D(3) but where Ca and Pi intake was not restricted. It appears from these findings that in horses, the increase of the Ca x Pi product in blood plasma during a Vitamin D intoxication contributes to the soft tissue calcifications. It is further concluded that in the event of a Vitamin D intoxication, it is recommended to restrict the Ca and Pi uptake immediately. The authors believe that this may help to prevent or at least diminish soft tissue calcifications which are often fatal to the horse due to nephrocalcinosis.

Animals↗
PubMedDate not supplied

Different shapes of the steroid hormone 1alpha,25(OH)(2)-vitamin D(3) act as agonists for two different receptors in the vitamin D endocrine system to mediate genomic and rapid responses.

Vitamin D(3) produces biologic responses as a consequence of its metabolism into 1alpha,25(OH)(2)-vitamin D(3) [1alpha,25(OH)(2)D(3)] and 24R,25(OH)(2)-vitamin D(3). The metabolic production of these two seco steroids and their generation of the plethora of biologic actions that are attributable to the parent vitamin D(3) are orchestrated via the integrated operation of the vitamin D endocrine system. This system is very similar in its organization to that of classic endocrine systems and is characterized by an endocrine gland (the kidney, the source of the two steroid hormones), target cells which possess receptors for the steroid hormones, and a feed-back loop involving changes in serum Ca(2+) that alter the secretion of parathyroid hormone (a stimulator of the renal 1-hydroxylase) which modulates the output by the kidney of the steroid hormones. There are, however, at least two unique aspects to the vitamin D endocrine system. (a) The chemical structures of vitamin D and its steroid hormones dictate that these be highly conformationally flexible molecules present a wide variety of shapes to their biologic environments. (b) It is now believed that 1alpha,25(OH)(2)D(3) produces biologic responses through two distinct receptors which recognize totally different shapes of the conformationally flexible 1alpha,25(OH)(2)D(3). Thus, the classic actions of 1alpha,25(OH)(2)D(3) to regulate gene transcription occur as a consequence of the stereospecific interaction of a modified 6-s-trans bowl-shape of 1alpha,25(OH)(2)D(3) with its nuclear receptor (VDR(nuc)). The ability of 1alpha,25(OH)(2)D(3) to generate a variety of rapid (seconds to minutes) biologic responses (opening of chloride channels, activation of PKC and MAP kinases) requires a planar 6-s-cis ligand shape which is recognized by a putative plasma membrane receptor (VDR(mem)) to initiate appropriate signal transduction pathways. This report summarizes the evidence for the specificity of different ligand shapes and the operation of the two receptor families for 1alpha,25(OH)(2)D(3).

Animals↗
PubMed2004

Calcium and vitamin D3 supplements in calcium and vitamin D3 sufficient early postmenopausal healthy women.

OBJECTIVE: To study the calcium homeostasis in healthy, calcium and vitamin D replete early postmenopausal women during oral supplementation with calcium and vitamin D3. DESIGN: A prospective, placebo-controlled, randomised, double-single-blind, 3-week study. SETTING: Outpatient clinic at Copenhagen University Hospital, Denmark. SUBJECTS: In all, 17 started, one was excluded. Totally, 16 healthy women, 45-61 y of age (mean 57.3 y) who were at least 4 y after menopause (mean 6.7 y) completed. INTERVENTIONS: All underwent three consecutive 7-day study periods. Each began with 4 days of normal diet followed by 3 days treatment of either C: one tablet of 1.250 mg calcium carbonate (ie 500 mg Ca2+ per tablet) twice daily (breakfast and dinner), or CD3: as in C but plus 400 IU vitamin D3 b.i.d., or P (only) placebo tablets b.i.d. RESULTS: At baseline plasma 25-hydroxycholecalciferol was normal (66+/-22 nmol/l) and the calcium intake without supplements 850 mg/day. In group C, the 24-h urinary calcium increased by 35% (6.9+/-2.0 mmol), vs the placebo group P (5.1+/-1.6 mmol) (P < 0.05). Addition of 800 IU vitamin D3 daily (CD3) did not increase calcium excretion further (6.6+/-2.1 mmol) but decreased plasma 1,25-(OH)2-vitamin D3 by 21% (P < 0.05). CONCLUSIONS: In this carefully controlled study calcium plus vitamin D3 supplements only had minor influences of uncertain significance on the calcium balance in healthy, calcium and vitamin D sufficient early postmenopausal women.

Administration, Oral↗
PubMed1981

Comparison of the appearance of radiolabelled vitamin D3 and 25-hydroxy-vitamin D3 in the chylomicron fraction of plasma after oral administration in man.

1. The uptake of either orally administered [3H]vitamin D3 or 25-[3H]hydroxy-vitamin D3 into the chylomicron fraction of plasma was studied in 12 healthy male subjects. 2. The amount of [3H]vitamin D3 in the chylomicron fraction expressed as a percentage of the total plasma radioactivity was higher than that of 25-[3H]hydroxy-vitamin D3. 3. It is suggested that the mechanism of intestinal absorption of vitamin D and 25-hydroxy-vitamin D may differ in man, the absorption of 25-hydroxy-vitamin D possibly being less dependent on bile acids.

Administration, Oral↗
PubMed1992

Serum levels of 1,25-(OH)2-vitamin D are not altered by long-term supplementation with alphacalcidol (1-OH-vitamin D3). A double-blind, placebo-controlled study.

The endogenous production of 1,25-(OH)2-vitamin D has been estimated to be 1.5 micrograms daily. Despite the use of alphacalcidol (1,25-(OH)2-vitamin D) during more than a decade the long-term effects of the serum levels of 1,25-(OH)2-vitamin D have been poorly investigated. When 1 microgram of alphacalcidol was given daily to 39 non-vitamin D deficient subjects in a double-blind, placebo-controlled study during 4 months no significant effects on the serum levels of 1,25-(OH)2-vitamin D or 25-(OH)-vitamin D were found. The treatment however induced a 50% increase in urinary excretion of calcium (p less than 0.01). In conclusion, long-term supplementation with a physiological dose of alphacalcidol does not influence the serum levels of 1,25-(OH)2-vitamin D, despite a marked effect on urinary calcium excretion.

Adult↗
PubMed1999

A liposomal model that mimics the cutaneous production of vitamin D3. Studies of the mechanism of the membrane-enhanced thermal isomerization of previtamin D3 to vitamin D3.

We reported previously that the rate of previtamin D3 (preD3) <==> vitamin D3 isomerization was enhanced by about 10 times in the skin compared with that in organic solvents. To elucidate the mechanism by which the rate of this reaction is enhanced in the skin, we developed a liposomal model that mimicked the enhanced isomerization of preD3 to vitamin D3 that was described in human skin. Using this model we studied the effect of changing the polarity of preD3 as well as changing the chain length and the degree of saturation of liposomal phospholipids on the kinetics of preD3 <==> vitamin D3 isomerization. We found that a decrease in the hydrophilic interaction of the preD3 with liposomal phospholipids by an esterification of the 3beta-hydroxy of preD3 (previtamin D3-3beta-acetate) reduced the rate of the isomerization by 67%. The addition of a hydroxyl on C-25 of the hydrophobic side chain (25-hydroxyprevitamin D3), which decreased the hydrophobic interaction of preD3 with the phospholipids, reduced the rate by 87%. In contrast, in an isotropic n-hexane solution, there was little difference among the rates of the conversion of preD3, its 3beta-acetate, and 25-hydroxy derivatives to their corresponding vitamin D3 compounds. We also determined rate constants (k) of preD3 <==> vitamin D3 isomerization in liposomes containing phosphatidylcholines with different carbon chain lengths. The rates of the reaction were found to be enhanced as the number of carbons (Cn) in the hydrocarbon chain of the phospholipids increased from 10 to 18. In conclusion, these results support our hypothesis that amphipathic interactions between preD3 and membrane phospholipids stabilize preD3 in its "cholesterol like" cZc-conformer, the only conformer of preD3 that can convert to vitamin D3. The stronger these interactions were, the more preD3 was likely in its cZc conformation at any moment and the faster was the rate of its conversion to vitamin D3.

1,2-Dipalmitoylphosphatidylcholine↗