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PubMed1968

Enzyme studies on the esterification of vitamin D in rat tissues.

1. The mechanism of vitamin D esterification in the rat was studied with liver, small-intestinal mucosa, pancreatic juice and blood plasma as enzyme sources and [1-(3)H]cholecalciferol, [U-(14)C]ergocalciferol and [4-(14)C]cholesterol as substrates. 2. No esterification of vitamin D could be detected with liver preparations nor with homogenates or acetone-dried powder extracts of intestinal mucosa. 3. Pancreatic juice esterified [1-(3)H]cholecalciferol with oleic acid, and specificity studies indicated that a cholesterol-esterifying enzyme was using vitamin D as substrate. 4. Plasma cholesterol-esterifying enzyme also esterified vitamin D. 5. The specificity of the esterification reaction is discussed in relation to (a) the molecular structure of the substrates and (b) their availability, in a micellar solution, to the enzyme. 6. It is concluded that cholesterol-esterifying enzymes esterify vitamin D in vivo during absorption from the small intestine and while it is transported in blood.

Animals↗

PubMed1979

Determination of vitamin D and its metabolites in plasma from normal and anephric man.

A multiple assay capable of reliably determining vitamins D(2) and D(3) (ergocalciferol and cholecalciferol), 25(OH)D(2) (25-hydroxyvitamin D(2)) and 25(OH)D(3) (25-hydroxyvitamin D(3)), 24,25(OH)(2)D (24,25-dihydroxyvitamin D), 25,26(OH)(2)D (25,26-dihydroxyvitamin D) and 1,25(OH)(2)D (1,25-dihydroxyvitamin D) in a single 3-5ml sample of human plasma was developed. The procedure involves methanol/methylene chloride extraction of plasma lipids followed by separation of the metabolites and purification from interfering contaminants by batch elution chromatography on Sephadex LH-20 and Lipidex 5000 and by h.p.l.c. (high-pressure liquid chromatography). Vitamins D(2) and D(3) and 25(OH)D(2) and 25(OH)D(3) are quantified by h.p.l.c. by using u.v. detection, comparing their peak heights with those of standards. 24,25(OH)(2)D and 25,26(OH)(2)D are measured by competitive protein-binding assay with diluted plasma from vitamin D-deficient rats. 1,25(OH)(2)D is measured by competitive protein-binding assay with diluted cytosol from vitamin D-deficient chick intestine. Values in normal human plasma samples taken in February are: vitamin D 3.5+/-2.5ng/ml; 25(OH)D 31.6+/-9.3ng/ml; 24,25(OH)(2)D 3.5+/-1.4ng/ml; 25,26(OH)(2)D 0.7+/-0.5ng/ml; 1,25(OH)(2)D 31+/-9pg/ml (means+/-s.d.). Values in two normal human plasma samples taken in February after 1 week of high sun exposure are: vitamin D 27.1+/-7.9ng/ml; 25(OH)D 56.8+/-4.2ng/ml; 24,25(OH)(2)D 4.3+/-1.6ng/ml; 25,26(OH)(2)D 0.5+/-0.2ng/ml. Values in anephric-human plasma are: vitamin D 2.7+/-0.8ng/ml; 25(OH)D 36.4+/-16.5ng/ml; 24,25(OH)(2)D 1.9+/-1.3ng/ml; 25,26(OH)(2)D 0.6+/-0.3ng/ml; 1,25(OH)(2)D was undetectable.

Animals↗

PubMed1992

Hypervitaminosis D associated with drinking milk.

BACKGROUND: Vitamin D has been added to milk in the United States since the 1930s to prevent rickets. We report the unusual occurrence of eight cases of vitamin D intoxication that appear to have been caused by excessive vitamin D fortification of dairy milk. METHODS: Medical records were reviewed and a dietary questionnaire was sent to eight patients who had unexplained hypervitaminosis D. Vitamin D analyses with high-performance liquid chromatography were performed on samples of the patients' serum, the dairy milk they drank, and the vitamin D concentrate added to the milk. RESULTS: All eight patients drank milk produced by a local dairy in amounts ranging from 1/2 to 3 cups (118 to 710 ml) daily. All had elevated serum 25-hydroxyvitamin D concentrations (mean [+/- SD], 731 +/- 434 nmol per liter [293 +/- 174 ng per milliliter]). Six of the eight patients had elevated serum vitamin D3 concentrations. Of the eight patients, seven had hypercalcemia and one had hypercalciuria but normocalcemia (mean serum calcium, 3.14 +/- 0.51 mmol per liter [12.6 +/- 2.1 mg per deciliter]). Analysis of the dairy's vitamin D-fortified milk revealed concentrations of vitamin D3 (cholecalciferol) that ranged from undetectable to as high as 232,565 IU per quart (245,840 IU per liter). An analysis of the concentrate that was used to fortify the milk, labeled as containing vitamin D2 (ergocalciferol), revealed that it contained vitamin D3. CONCLUSIONS: Hypervitaminosis D may result from drinking milk that is incorrectly and excessively fortified with vitamin D. Milk that is fortified with vitamin D must be carefully monitored.

Adult↗

PubMed1992

The vitamin D content of fortified milk and infant formula.

BACKGROUND: The fortification of milk and infant formula with vitamin D has had an important role in eliminating rickets in children and osteomalacia in adults. A recent outbreak of vitamin D intoxication caused by drinking milk fortified with excess vitamin D has led to questions about the level of vitamin D in milk from other producers. METHODS: We used high-performance liquid chromatography to measure vitamin D in samples of 13 brands of milk with various fat contents and 5 brands of infant formula purchased at random from local supermarkets in five Eastern states. RESULTS: Only 12 (29 percent) of the 42 samples of the 13 brands of milk and none of the 10 samples of the 5 brands of infant formula contained 80 to 120 percent of the amount of vitamin D stated on the label. Twenty-six of the 42 milk samples (62 percent) contained less than 80 percent of the amount claimed on the label. No vitamin D was detected in 3 of the 14 samples of skim milk tested (lower limit of assay, 4.7 IU per quart [5.0 IU per liter]). One milk sample labeled as containing vitamin D2 (ergocalciferol) contained vitamin D3 (cholecalciferol). Seven of the 10 samples of infant formula contained more than 200 percent of the amount stated on the label; the sample with the highest concentration contained 419 percent of the stated amount. None of the samples of infant formula contained less than the amount stated. CONCLUSIONS: Milk and infant-formula preparations rarely contain the amount of vitamin D stated on the label and may be either underfortified or overfortified. Since both underfortification and overfortification are hazardous, better monitoring of the fortification process is needed.

Animals↗

PubMed1999

Plasma 25-hydroxyvitamin D responses of younger and older men to three weeks of supplementation with 1800 IU/day of vitamin D.

OBJECTIVE: The objective of this study was to compare changes in plasma 25-hydroxyvitamin D (25(OH)D) levels of younger and older men after three weeks of oral vitamin D supplementation. METHODS: Nine younger men (22 to 28 years) and nine older men (65 to 73 years) with self-reported vitamin D intakes below 200 IU/d were enrolled in February and randomized to 1800 IU/d of ergocalciferol (vitamin D2, n=11) or to a control group (n=7) and followed for three weeks. Blood was collected at baseline, and after one, two and three weeks for measurement of plasma concentrations of total 25(OH)D, 25(OH)D2 and 25(OH)D3. RESULTS: In both the younger and older supplemented men, 25(OH)D2 and total 25(OH)D concentrations increased significantly during the study, whereas values of these metabolites did not change in younger or older control subjects. No group showed significant changes in 25-hydroxyvitamin D3. There was a significant interaction between age group and supplement group, suggesting that the effect of vitamin D2 supplementation on changes in 25(OH)D2 changes with age. The mean increase in 25(OH)D2 was greater in the younger supplemented men than in the older supplemented men (37+/-9 nmol/L vs. 19.5 nmol/L, p=0.027), and this accounted for their significantly greater increase in total 25(OH)D. CONCLUSION: These data are consistent with an age-related decline in the absorption, transport or liver hydroxylation of orally-consumed vitamin D.

Absorption↗

PubMed2006

Vitamin D supplementation and the prevention of fractures and falls: results of a randomised trial in elderly people in residential accommodation.

OBJECTIVES: To determine whether vitamin D supplementation reduces the risk of fracture or falls in elderly people in care home accommodation. DESIGN: A randomised controlled trial of cluster design. SETTING AND SUBJECTS: 223 Residential units (mainly identical 30-bedded units), within 118 homes for elderly people throughout Britain, with 3,717 participating residents (76% women, average age 85 years). The units provided mainly or entirely residential care (35% of residents), nursing care (42%) or care for elderly mentally infirm (EMI) residents (23%). METHODS: Participants were randomly allocated by residential unit (cluster design) to a treated group offered ergocalciferol 2.5 mg every 3 months (equivalent to a daily dose of 1,100 IU), or to a control group. Fractures were reported by staff and confirmed in hospital, and routinely collected data on reported falls were obtained. RESULTS: After median follow-up of 10 months (interquartile range 7-14 months), 64 (3.6%) of 1,762 vitamin D-treated residents and 51 (2.6%) of 1,955 controls had one or more non-vertebral fractures, and 24 (1.3%) and 20 (1.0%), respectively, had a hip fracture. The proportion reporting at least one fall was 44% in vitamin D-treated and 43% in control residents. The differences between the vitamin D and control groups were not statistically significant. The incidence of all non-vertebral fractures in the care homes (3.2% per year) and of hip fractures (1.1% per year) was low, similar to rates in elderly people in sheltered accommodation, and the pre-treatment serum 25-hydroxy vitamin D concentration was high [median 47 nmol/l, measured in a 1% (n = 18) sample]. CONCLUSIONS: We found no evidence that vitamin D prevents fractures or falls in elderly people in care home accommodation.

Accidental Falls↗

PubMed1977

Components of 25-hydroxyvitamin D in serum of young children in upper midwestern United States.

The relative importance of cholecalciferof (vitamin D3) and ergocalciferol (vitamin D2) in maintaining the vitamin D level in children (1/2 to 6 years old) living in the upper midwestern United States was determined by measurement of total 25-hydroxyvitamin D (25-OH-D), its components, and other indices of calcium homeostasis in serum. In 38 normal children, mean (range) serum total 25-OH-D was 32.8 (less than 5 to 53) ng/ml; in 25 of the 28 sera partitioned, the major component was 25-OH-D3. Significant seasonal variation in serum 25-OH-D3 (mean, range: 35.2, 17 to 51 ng/ml in summer and 15.9, less than 5 to 32 ng/ml in winter) was not accompanied by changes in mean serum 25-OH-D2, calcium, phosphorus, or alkaline phosphatase values. However, individual serum total 25-OH-D values correlated with serum phosphorus values (r = 0.37; P less than 0.05). The proportion of the total represented by 25-OH-D3 varied widely, with a a mean of 83% in summer and 67% in winter. Sources of D3, which include both dermal synthesis and intestinal absorption of D3 added to milk, appear to be more important than sources of D2 in maintaining vitamin D nutrition of young children throughout the year. However, sources of D2 offset the decrease in total 25-OH-D in winter months.

Alkaline Phosphatase↗

PubMed1987

Calcium and vitamin D supplements: effects on calcium metabolism in elderly people.

Calcium and vitamin D status were studied in 193 healthy elderly French people. Calcium intake was less than 500 mg/d in 62% of the patients and the vitamin D intake was less than 5 micrograms/d in all patients. They also exhibited reduced levels of serum calcium (SCa) and 25-hydroxyvitamin D (25-OHD) and high levels of parathyroid hormone (PTH) and alkaline phosphatase (SAP). The response to calcium (1000 mg/d) and ergocalciferol (20 micrograms/d) supplementation given for 6 mo was evaluated in 65 patients with 69 subjects taken as controls. The treatment induced a significant increase in SCa and in 25-OHD levels, and a subsequent decrease in PTH levels without modification of the mean calcitriol levels. The biochemical changes were more marked in long-stay hospital patients than in outpatients. All these changes were significantly different from those observed in the control group. Increasing the calcium and vitamin D intake reduces the biochemical signs of secondary hyperparathyroidism in elderly people.

Aged↗

PubMed1987

Intermittent high-dose vitamin D prophylaxis during infancy: effect on vitamin D metabolites, calcium, and phosphorus.

In infants receiving intermittent high dose vitamin D prophylaxis (600,000 IU ergocalciferol per dose orally) every 3-5 mo, the serum concentrations of vitamin D metabolites, calcium (Ca), and phosphorus (P) were determined before and 2 wk after each dose. The 25-hydroxyvitamin D (OHD) concentrations increased to well above normal but the values returned to the normal range before each subsequent dose. The 24,25- and 25,26-dihydroxyvitamin D ([OH]2D) levels followed a pattern similar to that of 25-OHD, and both were closely related to the latter (r = 0.85, p less than 0.005, and r = 0.84, p less than 0.005, respectively). The 1,25-(OH)2D concentrations did not vary in a consistent pattern and remained largely within the normal range. All infants had normal Ca levels before the first dose but 14 infants (34%) later had one or both Ca values above the upper normal limit of 2.80 mmol/L (2.81-3.32 mmol/L), indicating that the vitamin D doses were excessive despite the lack of accumulative increases in serum vitamin D concentrations.

24,25-Dihydroxyvitamin D 3↗

PubMed2000

Decreased bioavailability of vitamin D in obesity.

BACKGROUND: Obesity is associated with vitamin D insufficiency and secondary hyperparathyroidism. OBJECTIVE: This study assessed whether obesity alters the cutaneous production of vitamin D(3) (cholecalciferol) or the intestinal absorption of vitamin D(2) (ergocalciferol). DESIGN: Healthy, white, obese [body mass index (BMI; in kg/m(2)) > or = 30] and matched lean control subjects (BMI </= 25) received either whole-body ultraviolet radiation or a pharmacologic dose of vitamin D(2) orally. RESULTS: Obese subjects had significantly lower basal 25-hydroxyvitamin D concentrations and higher parathyroid hormone concentrations than did age-matched control subjects. Evaluation of blood vitamin D(3) concentrations 24 h after whole-body irradiation showed that the incremental increase in vitamin D(3) was 57% lower in obese than in nonobese subjects. The content of the vitamin D(3) precursor 7-dehydrocholesterol in the skin of obese and nonobese subjects did not differ significantly between groups nor did its conversion to previtamin D(3) after irradiation in vitro. The obese and nonobese subjects received an oral dose of 50000 IU (1.25 mg) vitamin D(2). BMI was inversely correlated with serum vitamin D(3) concentrations after irradiation (r = -0.55, P: = 0.003) and with peak serum vitamin D(2) concentrations after vitamin D(2) intake (r = -0.56, P: = 0.007). CONCLUSIONS: Obesity-associated vitamin D insufficiency is likely due to the decreased bioavailability of vitamin D(3) from cutaneous and dietary sources because of its deposition in body fat compartments.

Adult↗

PubMed1982

The biological activity of 25-hydroxycholecalciferol and 1,25--dihydroxycholecalciferol for rainbow trout (Salmo gairdneri).

Dietary 25-hydroxycholecalciferol (25-hydroxycholecalciferol (25-OH-D3) and 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] showed vitamin D activity in rainbow trout. However, inclusion of dietary cholecalciferol (vitamin D3 or D3), ergocalciferol (vitamin D2 or D2), 25-OH-D3 or 1,25-(OH)2D3 did not result in the presence of detectable levels of vitamin D or 25-OH-D in the blood plasma of the fish. Fish fed the diet devoid of vitamin D over an extended period of time showed symptoms of a droopy-tail or "lordosis-like" syndrome that appeared to be related to muscle weakness since x-ray examination indicated no abnormality in vertebral development. The requirement for vitamin D as cholecalciferol was in excess of 1600 IU/kg diet and may be as high as, or higher than 2400 IU/kg diet.

Animals↗

PubMed1984

Defective photoproduction of cholecalciferol in normal and uremic humans.

The initial step in cholecalciferol (vitamin D3) metabolism is the photo-conversion of 7-dehydrocholesterol to previtamin D3. This reaction occurs in the epidermis and requires ultraviolet light. We measured the circulating concentration of vitamin D (ergocalciferol and cholecalciferol), 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D in 14 normal white, 9 normal black subjects, and in 9 white and 17 black hemodialysis patients. The mean plasma vitamin D in normal white subjects was greater than in normal black subjects, 4.01 +/- 1.02 ng/ml versus 0.96 +/- 0.30 ng/ml, respectively (P less than 0.05). Plasma 25-hydroxyvitamin D in normal blacks was also less than in normal whites, 17.7 +/- 1.5 ng/ml versus 31.3 +/- 3.0 ng/ml, respectively (P less than 0.01). In uremic white subjects, plasma vitamin D, 6.7 +/- 2.6 ng/ml, was similar to normal white subjects. However, vitamin D was not detectable in 12 of 17 uremic black subjects and was depressed in the remainder of the group. Following exposure to a single minimal erythema dose of ultraviolet-B irradiation, the maximal increase in plasma vitamin D was depressed in white dialysis patients as compared to healthy white subjects, 6.3 +/- 1.9 ng/ml versus 21.3 +/- 2.8 ng/ml, respectively (P less than 0.02). 7-Dehydrocholesterol content was similar in epidermis from site-matched skin of fresh cadavers and white hemodialysis patients, 131 +/- 23 ng/mg versus 124 +/- 14 ng/mg skin, respectively. It is concluded that chronic hemodialysis patients exhibit defective photoproduction of cholecalciferol, despite normal epidermal content of substrate, 7-dehydrocholesterol.

Adult↗

PubMed1990

Relationship of membrane-bound sulfhydryl groups to vitamin D-stimulated uptake of [75Se]Selenite by the brush border membrane vesicles from chick duodenum.

The uptake of selenite by purified brush border membrane vesicles isolated from duodena of rachitic or vitamin D-treated chicks was studied by using radioactive selenite and a rapid filtration technique. Cholecalciferol treatment (500 IU at 72 h) significantly enhanced selenite uptake, a response that decreased when the vesicles were stored at room temperature for 2.5 h prior to the uptake measurement. Preincubation of the vesicles in 1.0 mmol/L H2O2 reduced [75Se]selenite uptake, indicating the involvement of oxidizable groups in the uptake reaction. Iodoacetic acid (IAA), a sulfhydryl-blocking reagent, at 1-2 mmol/L concentration eliminated the difference in selenite uptake due to cholecalciferol and had no effect on vesicles from rachitic animals. A higher concentration of IAA (10 mmol/L) enhanced selenite uptake manyfold and increased the absolute difference due to cholecalciferol treatment. Single intravenous doses of 100 IU cholecalciferol, 100 IU ergocalciferol, or 0.1 micrograms 1,25-dihydroxycholecalciferol also stimulated selenite uptake, suggesting a general response to vitamin D compounds. Normal animals given a single dose of 1,25-dihydroxycholecalciferol 12 h prior to killing also responded. Treatments that enhanced the uptake of [75Se]selenite also increased the amount of membrane-bound sulfhydryl groups, suggesting the involvement of membrane-bound sulfhydryl groups in the vitamin D response. A significant increase in selenite uptake by intravenous 1,25-dihydroxycholecalciferol occurred within 10 min. This rapid effect provides a new tool to probe early biochemical effects of vitamin D on intestinal epithelium.

Animals↗

PubMed2004

Effect of vitamin D2- and D3-enriched diets on egg vitamin D content, production, and bird condition during an entire production period.

Vitamin D insufficiency during winter is a common problem for humans in Europe. One way to ease this problem is through the production of vitamin D-fortified eggs. To evaluate such a production process, the effects of vitamin D supplementation during an entire production period were assessed. Transfer of vitamin D3 (cholecalciferol) and vitamin D2 (ergocalciferol) from the diet to egg yolks was measured using 2 different levels of both vitamins (6,000 and 15,000 IU/kg feed) relative to a control treatment (2,500 IU vitamin D3/kg feed). During the experiment, production parameters, egg quality (egg weight, Haugh unit, specific gravity, eggshell fracture force, and Ca content of eggshell), and the condition of hens were monitored. At the end of the experiment histopathological tests were performed. Supplementing diets with vitamin D3 increased egg yolk vitamin D content more effectively than did supplementation with vitamin D2. For groups of hens receiving 6,000 or 15,000 IU of vitamin D3/kg feed, egg yolk vitamin D3 content ranged from 9.1 to 13.6 and from 25.3 to 33.7 microg/100 g, respectively. Corresponding values for birds fed vitamin D2 were 4.7 to 7.0 and 13.3 to 21.0 microg/100 g. Both supplements enhanced vitamin D3 content of egg yolks relative to the control diet (2.5 to 5.0 microg/100 g of egg yolk). Vitamin D supplements had no effects on production parameters compared with the control diet. However, especially vitamin D3 improved bone strength (P < 0.05). Autopsy at the end of the experiment indicated no detrimental accumulation of calcium in the kidneys, liver, heart, muscles, or lungs.

Animals↗

PubMed1997

Role of calcium in modulation of toxicities due to cisplatin and its analogs: a histochemical approach.

Cisplatin, carboplatin and paclitaxel (taxol) are potent antineoplastic agents with associated toxicities, especially gastrointestinal and nephrotoxicity that are their dose-limiting factors in clinical oncology. In an attempt to elucidate their mechanism(s) of toxicity, liver and kidney tissues from normal and drug treated rats and dogs were evaluated for changes in various dehydrogenase and non-specific lipase enzymes. Histochemically, cisplatin treatment induced an inhibition of all the enzymes studied except glucose-6-phosphate dehydrogenase and non-specific lipases, where there was a significant increase. Supplemental treatments with calcium [1 ml of 1.3% CaCl2/day in rats and 2.50 mg (150000 USP units) ergocalciferol plus 1000 mg of elemental calcium as TUMS 500 (EffeCal)/day in dogs] seem to protect against severe gastrointestinal toxicity and nephrotoxicity.

Adenosine Triphosphate↗

PubMedDate not supplied

Calcium, magnesium, and psychotic symptoms in a girl with idiopathic hypoparathyroidism.

A case of psychosis due to idiopathic hypoparathyroidism (IHP) has been followed for over 9 years. The optimal treatment for IHP psychosis was found to be a combination of ergocalciferol and fairly large doses of antipsychotic medication. In general, psychotic episodes occurred when there was hypocalcemia, hypercalcemia, or hypomagnesemia. Antipsychotic medication was not efficacious unless serum calcium and magnesium levels were both normal. It is suggested that psychiatric disturbances in hypoparathyroidism and treatment resistance to antipsychotic medication in other functional psychoses may also be related to hypomagnesemia.

Adolescent↗

PubMed1979

The relevance of 25-hydroxycalciferol measurements in the treatment of hypoparathyroidism.

In twenty-one patients with chronic hypoparathyroidism a close correlation was observed between the prescribed dose of ergocalciferol and mean serum 25-hydroxycalciferol levels. In the 75 serum specimens examined, a significant correlation was found between 25-hydroxycalciferol levels and calcium concentrations. The measurement of serum 25-hydroxycalciferol levels is of potential clinical value in the prediction of hyper- or hypocalcaemic episodes and in monitoring patient compliance.

Adolescent↗

PubMed1995

Functional improvement with vitamin D replenishment in a cohort of frail, vitamin D-deficient older people.

OBJECTIVE: To evaluate functional improvement in a population of frail, homebound older persons with low vitamin D status as vitamin D stores improve. DESIGN: Randomized, controlled intervention study. SETTING: Subjects' homes and a nursing facility in Baltimore, Maryland. PARTICIPANTS: The first 32 subjects (community-dwelling, homebound older subjects from the Johns Hopkins Elder Housecall Program and nursing home residents from the Johns Hopkins Geriatrics Center) entered in a longitudinal study of vitamin D replacement. MEASUREMENTS: Baseline 25-hydroxyvitamin D levels were measured and repeated at least 1 month after therapy with either placebo or vitamin D (ergocalciferol). Subjects were also administered the Frail Elderly Functional Assessment (FEFA) questionnaire, an instrument demonstrated to be reliable, valid, and sensitive to small increments of functional change in this population. MAIN RESULTS: All subjects started with 25-hydroxyvitamin D levels less than 15 ng/mL. Those subjects whose levels improved by at least 3 ng/mL (> assay coefficient of variation) also demonstrated improvement in FEFA score. Regression analysis between change in FEFA score compared with change in 25-hydroxyvitamin D was significant (r = .4; P = .02). CONCLUSIONS: In this cohort of homebound older people, improvement in vitamin D status was associated with functional improvement as measured by the FEFA questionnaire.

Aged↗