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Vitamin D nutrition and vitamin D metabolism in the premature human neonate.

The effect of supplementation with daily doses of vitamin D2 (1000 IU or 3000 IU, 25-75 micrograms, 63-189 nmol) has been studied in 39 premature neonates, initial gestational age 25-32 weeks. The initial mean plasma 25-hydroxyvitamin D was 25.8 nmol/l (10.3 ng/ml) but in 12 infants, most of whom were born in the winter months, the level was less than 15 nmol/l (6 ng/ml), and in seven babies plasma 1,25-dihydroxyvitamin D was less than 48 pmol/l (20 pg/ml). These findings suggest a considerable degree of maternal vitamin D-deficiency. Maximum attained concentrations of 25-hydroxyvitamin D on treatment were 77.3 nmol/l (30.9 ng/ml), high dose and 86.8 nmol/l (34.7 ng/ml), low dose, the mean rate of increase was greatest during the first two weeks (2.2 nmol/l/d; 0.88 ng/ml/d) and declined over the next 4 weeks. Mean maximum concentrations of 1,25-dihydroxyvitamin D2 were 283 pmol/l, (121 pg/ml), high dose and 309 pmol/l (129 pg/ml), low dose. Apart from a minor contribution to the initial plasma 1,25-dihydroxyvitamin D concentration, no effect of gestational age could be discerned in any of the measured variables. The endogenous pool of 1,25-dihydroxyvitamin D3 decayed with a T 1/2 of 22.5 d, indicating that vitamin D supplementation of these infants was necessary to avoid vitamin D-deficiency.

Calcifediol↗

Antioxidant functions of vitamins. Vitamins E and C, beta-carotene, and other carotenoids.

Tocopherols and tocotrienols (vitamin E) and ascorbic acid (vitamin C) as well as the carotenoids react with free radicals, notably peroxyl radicals, and with singlet molecular oxygen (1O2), this being the basis of their function as antioxidants. RRR-alpha-tocopherol is the major peroxyl radical scavenger in biological lipid phases such as membranes or low-density lipoproteins (LDL). L-Ascorbate is present in aqueous compartments (e.g. cytosol, plasma, and other body fluids) and can reduce the tocopheroxyl radical; it also has a number of metabolically important cofactor functions in enzyme reactions, notably hydroxylations. Upon oxidation, these micronutrients need to be regenerated in the biological setting, hence the need for further coupling to nonradical reducing systems such as glutathione/glutathione disulfide, dihydrolipoate/lipoate, or NADPH/NADP+ and NADH/NAD+. Carotenoids, notably beta-carotene and lycopene as well as oxycarotenoids (e.g. zeaxanthin and lutein), exert antioxidant functions in lipid phases by free-radical or 1O2 quenching. There are pronounced differences in tissue carotenoid patterns, extending also to the distribution between the all-trans and various cis isomers of the respective carotenoids. Antioxidant functions are associated with lowering DNA damage, malignant transformation, and other parameters of cell damage in vitro as well as epidemiologically with lowered incidence of certain types of cancer and degenerative diseases, such as ischemic heart disease and cataract. They are of importance in the process of aging. Reactive oxygen species occur in tissues and cells and can damage DNA, proteins, carbohydrates, and lipids. These potentially deleterious reactions are controlled in part by antioxidants that eliminate prooxidants and scavenge free radicals. Their ability as antioxidants to quench radicals and 1O2 may explain some anticancer properties of the carotenoids independent of their provitamin A activity, but other functions may play a role as well. Tocopherols are the most abundant and efficient scavengers of peroxyl radicals in biological membranes. The water-soluble antioxidant vitamin C can reduce tocopheroxyl radicals directly or indirectly and thus support the antioxidant activity of vitamin E; such functions can be performed also by other appropriate reducing compounds such as glutathione (GSH) or dihydrolipoate. The biological efficacy of the antioxidants is also determined by their biokinetics.

Animals↗

Abnormal concentrations of B vitamins and amino acids in plasma and B vitamins in bile of rabbits with aflatoxicosis.

The dosages of aflatoxin B1 (AFB1) required to produce significant changes in concentrations of B vitamins in plasma and bile and of amino acids in plasma of rabbits were determined. Folate increased by 98% in plasma, whereas concentration of thiamine, vitamin B6, and biotin decreased by more than 50%. In bile, choline and biotin increased 14- and 18-fold, respectively, whereas folate and niacin decreased by more than 50%. All amino acids in plasma increased between 76 and 155%. The dosages of AFB1 required to induce these changes were usually between 12.5 and 37.5 microgram/kg of body weight per day. Except for changes in biliary concentrations of pantothenic acid, folic acid, and biotin, lower threshold dosages of aflatoxin were required to produce weight loss and anorexia (5.0 and 8.5 microgram of AFB1/kg per day, respectively) than for changes in vitamins and amino acids (approximately 25 to 50 microgram of AFB1/kg per day). The data indicated that AFB1 interfered with the metabolism of B vitamins and amino acids in rabbits.

Aflatoxin B1↗

Comparison of effect of vitamin E-coated dialyzer and oral vitamin E on hemodialysis-induced Cu/Zn-superoxide dismutase.

BACKGROUND: We reported earlier that production of Cu/Zn-superoxide dismutase (SOD) increases markedly in hemodialysis patients but not in non-dialyzed chronic renal failure (CRF) patients. In this study, we compared the antioxidant effects of oral vitamin E supplementation (VE-PO) and vitamin E coating of a dialyzer (VE-BMD) by measuring increased Cu/Zn-SOD in hemodialysis patients. METHODS: 31 hemodialysis patients were divided into two groups: 16 hemodialysis patients underwent usual dialysis with vitamin E supplementation 600 mg/day while 15 others were dialyzed using vitamin E-coated membrane for 6 months. Total plasma SOD activity was determined by NBT method, plasma Cu/Zn-SOD contents by ELISA and Cu/Zn-SOD mRNA in leukocytes by RT-PCR. RESULTS: VE-PO and VE-BMD showed almost comparable effects on Cu/Zn-SOD contents and its mRNA levels in hemodialysis patients. VE-PO resulted in a progressive decrease of Cu/Zn-SOD content (p < 0.001). A comparable progressive decrease was observed also in VE-BMD (p < 0.0001). Both VE-PO and VE-BMD resulted in a progressive decrease of Cu/Zn-SOD mRNA (p < 0.01), which reached the level of non-dialyzed CRF patients.

Administration, Oral↗

Calcium and vitamin D metabolism in hypocalcemic vitamin D-resistant rickets carriers.

BACKGROUND/AIMS: Hypocalcemic vitamin D-resistant rickets (HVDRR) is a rare monogenic autosomal recessive disorder associated with mutations in the gene of the vitamin D receptor (VDR), the mediator of 1,25(OH)2D3 action. Although many investigations have discussed the clinical manifestations and molecular etiology of this disease, only a few have investigated the biochemical and hormonal status of heterozygous HVDRR. The aim of the current work was to investigate the profile of selected biochemical and hormonal parameters related to the vitamin D endocrine system in a large number of HVDRR heterozygotes. METHODS: 67 relatives of 2 HVDRR patients, all members of an extended Greek kindred of five generations with a common ancestor, were included in the study. Direct sequencing was used to identify VDR gene mutations. Serum Ca, P, 25(OH)D, iPTH, and 1,25(OH)2D levels were determined in all members of the kindred. RESULTS: DNA analysis of the participants led to the design of two study groups: the HVDRR carriers (24) and the control subjects (43). Our results showed elevated circulating serum levels of 1,25(OH)2D3 and lower levels of PTH than their age- and sex-matched controls. No hypocalcemia or hypophosphatemia were detected in HVDRR carriers. CONCLUSIONS: Our findings suggest that HVDRR carriers may have compensatory elevated serum levels of 1,25(OH)2D3 through which they restrain PTH secretion. The study of HVDRR carriers could be a useful tool for the investigation of the vitamin D endocrine system.

Adolescent↗

Vitamin D and epidermal differentiation: evidence for a role of endogenously produced vitamin D metabolites in keratinocyte differentiation.

Vitamin D3 is produced in the skin. It is metabolized primarily in the liver to the major circulating form 25-hydroxy vitamin D3, [25(OH)D3] which is metabolized in the kidney to produce the biologically active form of the hormone, 1,25-dihydroxy vitamin D3, [1,25(OH)2D3]. The skin not only participates in the production of vitamin D3 but also contains receptors for 1,25(OH)2D3 suggesting a role of this hormone in the growth and differentiation of this tissue. 1,25(OH)2D3 appears to play a role in epidermopoiesis and melanin pigmentation. Recently, using cultures of neonatal human foreskin keratinocytes, we have demonstrated that these cells produce abundant quantities of 1,25(OH)2D3 from 25(OH)D3. The production of 1,25(OH)2D3 varies with the degree of differentiation of keratinocytes and is regulated by exogenous 1,25(OH)2D3. 1,25(OH)2D3 induces differentiation possibly because of its ability to increase intracellular free calcium levels. A tentative model is provided to demonstrate potential mechanisms by which 1,25(OH)2D3-induced changes in intracellular calcium could regulate epidermal differentiation.

Animals↗

Inhibition of the binding of 7,12-dimethylbenz [alpha] anthracene to DNA of murine epidermal cells in culture by vitamin A and vitamin C.

The effects of various derivatives of vitamin A and vitamin C on the binding of (3H)DMBA to murine epidermal cells (MEC) DNA in culture has been investigated. All-trans-retinoic acid, retinol, and retinol acetate inhibit the binding of DMBA to DNA at the nontoxic doses while 13-cis-retinoic acid dose not significantly modulate the binding of the carcinogen to DNA. Vitamin C, as well as its salt, also significantly reduces the binding of DMBA to DNA. Thus, the antitumorigenic effect of vitamins A and C may also be related to their ability to inhibit the binding of active metabolites of carcinogen to cellular DNA.

9,10-Dimethyl-1,2-benzanthracene↗

Vitamin C protects human arterial smooth muscle cells against atherogenic lipoproteins: effects of antioxidant vitamins C and E on oxidized LDL-induced adaptive increases in cystine transport and glutathione.

Glutathione (GSH) plays a key role in cellular antioxidant defenses by scavenging reactive oxygen species and reducing lipid peroxides. Intracellular GSH levels are regulated by transport of its precursor L-cystine via system xc-, which can be induced by oxidant stress. As oxidatively modified low density lipoproteins (LDLs) contribute to impaired vascular reactivity and the formation of atherosclerotic lesions, we have examined the effects of oxidized LDL and the antioxidant vitamins C and E on the L-cystine-GSH pathway in human umbilical artery smooth muscle cells (HUASMCs). Oxidized LDL, but not native LDL, elevated intracellular GSH levels and L-cystine transport via system xc- in a time-dependent (up to 24 hours) and dose-dependent (10 to 100 microg x mL-1) manner. These increases were dependent on protein synthesis and the extent of LDL oxidation, but the induction of L-cystine transport activity was independent of GSH synthesis. Pretreatment of HUASMCs for 24 hours with vitamin E (100 micromol/L) attenuated oxidized LDL-mediated increases in GSH, whereas pretreatment with vitamin C depressed basal levels and abolished oxidized LDL-induced increases in GSH and L-cystine transport in a time-dependent (3 to 24 hours) and dose-dependent (10 to 100 micromol/L) manner. Pretreatment of cells with dehydroascorbate had no effect on oxidized LDL-mediated increases in L-cystine transport and only marginally attenuated increases in GSH. Our findings provide the first evidence that vitamin C spares endogenous adaptive antioxidant responses in human vascular smooth muscle cells exposed to atherogenic oxidized LDL.

Antioxidants↗

A new active vitamin D, ED-71, increases bone mass in osteoporotic patients under vitamin D supplementation: a randomized, double-blind, placebo-controlled clinical trial.

CONTEXT: ED-71 has been shown to increase lumbar bone mineral density (BMD) in osteoporotic subjects. However, vitamin D insufficiency might have influenced the effect of ED-71 on BMD. OBJECTIVE: Our objective was to examine whether ED-71 can increase BMD in osteoporotic patients under vitamin D supplementation. DESIGN, SETTING, AND PATIENTS: We conducted a randomized, double-blind, placebo-controlled clinical trial of 219 osteoporotic patients (49-87 yr of age). INTERVENTIONS: Subjects were randomly assigned to receive placebo or 0.5, 0.75, or 1.0 microg/d ED-71 for 12 months. All the subjects received 200 or 400 IU/d vitamin D(3). MAIN OUTCOME MEASURES: We assessed changes in lumbar and hip BMD and bone turnover markers from baseline. RESULTS: Lumbar BMD increased with ED-71 treatment for 12 months (2.2, 2.6, and 3.1% from baseline and 2.9, 3.4, and 3.8% vs. placebo group in subjects receiving 0.5, 0.75, and 1.0 microg ED-71, respectively). Total hip BMD also increased with 0.75 and 1.0 microg ED-71 (-0.8, 0.6, and 0.9% from baseline and 0.1, 1.5, and 1.8% vs. placebo group in the 0.5, 0.75, and 1.0 microg ED-71 groups, respectively). Bone formation and resorption markers were suppressed by approximately 20% after 12 months of 0.75 and 1.0 microg ED-71 treatment. Transient hypercalcemia over 2.6 mmol/liter occurred in 7, 5, and 23% of subjects in the 0.5, 0.75, and 1.0 microg ED-71 groups, respectively, but none of them developed sustained hypercalcemia. CONCLUSIONS: These results demonstrate that ED-71 treatment at around 0.75 microg/d can effectively and safely increase lumbar and hip BMD in osteoporotic patients with vitamin D supplementation.

Absorptiometry, Photon↗

The N-terminal domain of transcription factor IIB is required for direct interaction with the vitamin D receptor and participates in vitamin D-mediated transcription.

The interaction of the vitamin D receptor (VDR) with transcription factor IIB (TFIIB) represents a potential physical link between the VDR-DNA complex and the transcription preinitiation complex. However, the functional relevance of the VDR-TFIIB interaction in vitamin D-mediated transcription is not well understood. In the present study, we used site-directed mutagenesis to demonstrate that the structural integrity of the amino-terminal zinc finger of TFIIB is essential for VDR-TFIIB complex formation. Altering the putative zinc-coordinating residues (C15, C34, C37, or H18) to serines abolished TFIIB interaction with the VDR as assessed in a yeast two-hybrid system and by in vitro protein interaction assays. This N-terminal, VDR-interactive domain functioned as a selective, dominant-negative inhibitor of vitamin D-mediated transcription. Expressing amino acids 1-124 of human TFIIB (N-TFIIB) in COS-7 cells or in osteoblastic ROS17/2.8 cells effectively suppressed 1,25-dihydroxyvitamin D3 (1,25-(OH)2D3)-induced transcription, but had no effect on basal or glucocorticoid-activated transcription. A mutant N-terminal domain [N-TFIIB(C34S:C37S)] that does not interact with VDR had no impact on 1,25-(OH)2D3-induced transcription. Interestingly, both in vitro and in vivo protein interaction assays showed that the VDR-TFIIB protein complex was disrupted by the 1,25-(OH)2D3 ligand. Mechanistically, these data establish a functional role for the N terminus of TFIIB in VDR-mediated transcription, and they allude to a role for unliganded VDR in targeting TFIIB to the promoter regions of vitamin D-responsive target genes.

Amino Acid Sequence↗

Effects of oral administration of "rumen-bypass" vitamin D3 on vitamin D and calcium metabolism in periparturient cows.

Eleven late-pregnant Jersey cows were assigned to two groups; a group (PO-RBVD group) consisting of five cows treated with an oral administration of 10 million I.U. of an encapsulated form of vitamin D3 ("rumen-bypass" VD3; RBVD3) and another group (IMVD group) consisting of the other six treated with an intramuscular injection of 10 million I.U. of vitamin D3 (VD3). The cows received the RBVD3 or VD3 administration at 7 days before the expected parturition. The changes in the plasma concentrations of vitamin D metabolites, ionized Ca (Ca++) and inorganic phosphorus (iP) were evaluated. Of the vitamin D metabolites, the plasma 25-hydroxyvitamin D concentrations in PO-RBVD group increased significantly after the RBVD3 administration and remained in high levels that were significantly higher than those in IMVD group. This suggested that RBVD3 was absorbed rapidly and excellently from the post-ruminal digestive tract without the degradation by ruminal microorganisms. The plasma Ca++ and iP concentrations in PO-RBVD group tended to be higher after the administration and around parturition than those in IMVD group. From these observations, it was suggested the oral RBVD3 administration had more potent ability to prevent parturient paresis compared with the VD3 injection used widely in Japan.

Administration, Oral↗

Differential effects of 20-epi vitamin D analogs on the vitamin D receptor homodimer.

Vitamin D analogs have received increased attention because of their possible therapeutic benefits in treating osteoporosis and various proliferative disorders. Several analogs were examined for their effects on DNA binding of the vitamin D receptor (VDR) homodimer complex with the murine osteopontin vitamin D response element. All of the tested analogs increased complex binding by recombinant human VDR in the electrophoretic mobility shift assay and notable differences in mobility of these complexes were observed. A panel of C-terminal anti-VDR antisera were screened for their ability to interact with analog-bound VDR homodimer complexes or as a heterodimer complex with recombinant human retinoid X receptor alpha (rhRXR alpha). Like calcitriol, analog-bound heterodimer complexes were largely resistant to interaction with these antisera; however, striking differences were observed with the various antisera in an analogous homodimer binding experiment. KH1060 and CB1093, analogs with 20-epi conformations, produced homodimer complexes that were 3- to 6-fold more resistant to supershifting with Ab180 compared with the hormone or EB1089. Chymotrypsin digestion in combination with Western blotting using a C-terminal anti-VDR antiserum revealed similar digestion patterns for all ligands. However, KH1060- and CB1093-bound VDR complexes were more resistant to digestion than either calcitriol or EB1089. Finally, the ability of these compounds to yield stable homodimer complexes was assessed by challenging preformed homodimer with the exogenous addition of rhRXR alpha extracts. Although new heterodimer complexes appeared in a time-dependent fashion, the preformed homodimer complexes exhibited stable binding throughout the time course of the experiment. The results indicate that VDR homodimers are targets of vitamin D analogs with differential effects on C-terminal protein conformation that may partially explain the varied biological responses of these compounds.

Amino Acid Sequence↗

Inhibition of benzo(a)pyrene-induced carcinogenesis by vitamin C alone and by vitamin C/vitamin E and selenium/glutathione.

The reduction on peroxidation caused by benzopyrenes by some naturally occurring antineoplastic agents was studied in this experimental work. Inhibition/reduction of experimental carcinogenesis induced by benzo(a)pyrene by vitamin C alone and by vitamin C/vitamin E and selenium/ glutathione was attempted in 224 female Wistar rats divided in four groups. Injected with 10.08 mL benzo(a)pyrene, the animals were treated with some naturally occurring substances like vitamin C alone and a combination of anticarcinogens. By calculating the carcinogenic potency of benzo(a)pyrene and the anticarcinogenic potency of substances used as well as histological examination of developed tumors and survival time of treated animals, it was found that vitamin C exerts a significant anticarcinogenic effect of 8.3 units and that the combination of the two anticarcinogens used produced a significant prolongation of the animals survival time with anticarcinogenic potency of 22.1 and 22.2 units, respectively. This is considered a potent anticarcinogenic effect. The question of an additional supportive administration of such agents complementary to the conventional cancer chemotherapy in humans is raised. Of course, further studies are needed.

Animals↗

Secondary hyperparathyroidism and vitamin D receptor binding to vitamin D response elements in rats with incipient renal failure.

The pathogenesis of secondary hyperparathyroidism in early renal failure is poorly understood. In the study presented here, parathyroid hormone and GFR in rats with mild renal failure of various durations are evaluated. Parathyroid hormone increased significantly 3 days after nephrectomy and peaked at 2 wk, despite reduction in GFR of < 50%. Parathyroid hormone remained elevated, but there was no difference in serum levels of calcium, phosphorus, and calcitriol between the nephrectomized and sham-operated rats. There were also no differences in both intestinal and kidney vitamin D receptor concentrations between the two groups. Histomorphometric analysis of bone at 6 wk revealed significant increase in osteoid thickness, osteoblast number, erosion surface with osteoclasts, and erosion depth. Employing electrophoretic mobility shift assay, we consistently observed a significant reduction in kidney calcitriol-receptor complex binding to mouse osteopontin vitamin D response element (-70.2 +/- 4.9%, P < 0.001). Western blot analysis also revealed a significant reduction in at least one retinoid X receptor isoform. In conclusion, biochemical and histological evidence of secondary hyperparathyroidism develops in rats with mild renal failure, despite normal calcium, phosphorus, calcitriol, and vitamin D receptor concentrations. These rats also have evidence of reduced renal vitamin D receptor binding to nuclear response elements. This finding, possibly an important early factor in the pathogenesis of secondary hyperparathyroidism, could also play a role in the development of compensatory renal growth of the remnant kidney.

Animals↗

Treatment with vitamin D3 and/or vitamin K2 for postmenopausal osteoporosis.

It is established in Japan that treatment with 1alpha-hydroxyvitamin D3 (alfacalcidol) slightly reduces bone turnover, sustains lumbar bone mineral density (BMD), and prevents osteoporotic vertebral fractures in postmenopausal women with osteoporosis, while vitamin K2 (menatetrenone) enhances gamma-carboxylation of bone glutamic acid residues and secretion of osteocalcin, sustains lumbar BMD, and prevents osteoporotic fractures in patients with osteoporosis. Available evidence suggests that the effect of vitamin K2 on mineralization by human periosteal osteoblasts is enhanced in the presence of 1,25 dihydroxyvitamin D3 in vitro. The effect of vitamin K2 on BMD in ovariectomized rats is affected by the plasma 25-hydroxyvitamin D3 level in vivo, and is significant only when rats are fed a diet containing vitamin D3. Based on this line of evidence, combined treatment with alfacalcidol and menatetrenone for osteoporosis is surmised to be more effective than treatment with menatetrenone alone, and may have anabolic effects on osteoporotic bone. This combined treatment may increase bone formation as well as bone resorption over the mild anti-resorptive effect of alfacalcidol itself, and shows the greatest effect on lumbar BMD or the incidence of vertebral fractures in studies in which the mean age and years since menopause of subjects were low and the degree of osteoporosis was mild. It may be effective for mild postmenopausal osteoporosis in which age-related deterioration of trabecular bone properties remains below the threshold for vertebral fractures, even if bone resorption is increased and trabecular bone has deteriorated.

Animals↗

The cytotoxic effect of the vitamin B12 inhibitor cyanocobalamin [c-lactam], and a review of other vitamin B12 antagonists.

The vitamin B12 antagonist cyanocobalamin [c-lactam] was cytotoxic to cultured human leukemia cells, grown in methylfolate, homocysteine, and vitamin B12, but not in the presence of methionine. Small concentrations of methionine were effective in restoring the growth rate in a dose-dependent fashion, confirming methionine deficiency as the cytotoxic principle. Cyanocobalamin [c-lactam] prevented utilization of the methyl group of methylfolate, but no evidence of folate deficiency developed in long-term culture. High concentrations of non-methylated folate were unable to reverse the cytotoxicity, excluding a methylfolate 'trap' as the cause. Low concentrations of serine in the medium induced transient biochemical megaloblastosis. Cyanocobalamin [c-lactam] caused this to occur earlier, and persist. In high concentrations of serine, the inhibitor caused only transient changes in deoxyuridine suppression. Homocysteine cannot be remethylated without vitamin B12, and condensation with serine is the only other excretory pathway for this toxic amino acid. We hypothesize that impaired DNA synthesis in vitamin B12 deficiency is the result of diverting serine away from thymidylate synthesis, into homocysteine metabolism.

5-Methyltetrahydrofolate-Homocysteine S-Methyltran↗

The differences of the metabolism related to vitamin B6-dependent enzymes among vitamin B6-deficient germ-free and conventional rats.

The differences of the metabolism related to vitamin B6-dependent enzymes were investigated using germ-free and conventional rats. There was a significant difference in the boyd weight gain between vitamin B6-deficient germ-free and conventional rats after about 30 days of the experiment, and the body weight gain was much less in the deficient germ-free rats than in the deficient conventional ones. Urinary excretion of xanthurenic acid was higher in the deficient germ-free rats than in the deficient conventional ones after 18 days. There was a significant difference in the activities of kynurenine aminotransferase in mitochondrial fractions of germ-free rats, but not in mitochondrial fractions of conventional ones. The activities of aspartate and alanine aminotransferases, with or without pyridoxal phosphate, significantly decreased in the deficient germ-free rats, but not in the deficient conventional ones. These findings indicate that the degree of vitamin B6 deficiency was more severe in the deficient germ-free rats than in the deficient conventional ones, and also suggest that intestinal microflora may have some effects on vitamin B6-deficient conventional rats.

Alanine Transaminase↗

Demonstration of a vitamin B12 binder in pancreatic juice. Effect on the intestinal uptake of vitamin B12.

Determination of vitamin-B12-binding capacity and gel filtration of human pancreatic juice (HPJ) and rat pancreatic juice (RPJ) demonstrated a vitamin B12 binder different from gastric intrinsic factor (IF). The results also indicated the presence of the pancreatic B12 binding in human duodenal juice. The binder in RPJ had no significant effect on the uptake of 57CoB12 and 57CoB12 bound to rat IF by perfused rat intestinal segments (p greater than 0.5; p greater than 0.1). The binder in HPJ had no effect on the uptake of unbound 57CoB12 or 57CoB12 bound to human IF by guinea pig intestinal brush borders (p greater than 0.05; p greater than 0.1). The results indicate that the pancreatic vitamin B12 binder does not influence the intestinal uptake of vitamin B12.

Animals↗