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PubMed1978

Intestinal cholecalciferol absorption in the elderly and in younger adults.

1. A method for assessing cholecalciferol absorption in man is described. 2. The intestinal absorption of [3H]cholecalciferol was studied in 20 female geriatric patients, most of whom were vitamin D-depleted. 3. The plasma [3H]cholecalciferol response after oral ingestion was significantly lower than that of a group of younger female subjects. 4. The plasma response of labelled polar metabolites of cholecalciferol was also lower in the geriatric than in the younger group, suggesting that increased removal of label by conversion into more polar metabolites could not account for the reduced plasma [3H]cholecalciferol response. 5. There was no evidence that alteration in gastrointestinal motility could account for the different rate of appearance of the labelled vitamin in the plasma in the two groups. 6. It is suggested that there is a defect in intestinal absorption of cholecalciferol in the elderly.

Adult↗
PubMed1991

The effects of dietary levels of inorganic phosphorus, calcium and cholecalciferol on the digestibility of phytate-P by the chick.

Male broiler chicks (1-d-old; Ross one) were given either a control diet containing recommended levels of phosphorus, calcium and cholecalciferol or experimental diets low in P and with variable levels of Ca (normal and low) and cholecalciferol (normal or high). The low-P diet with normal levels of Ca and cholecalciferol induced a hypophosphataemia and a hypercalcaemia which was reflected in reduced tibia length and weight and in reduced Ca, P and magnesium contents of tibia. The phytate digestibility remained normal while the retention of P and Ca fell significantly. The lowering of Ca alone elevated phytate digestibility and restored P and Ca retention. The hypercalcaemia and hypophosphataemia remained and tibia mineralization remained impaired. The raising of cholecalciferol alone dramatically increased phytate digestibility and the retention of Ca and P. While this remedied the hypercalcaemia, the hypophosphataemia persisted as did the diminution of tibia weight. The simultaneous lowering of dietary Ca and elevation of cholecalciferol on low-P diets restored all variables to the levels for the control diet. Circulating levels of 1,25-dihydroxycholecalciferol were significantly elevated by low-P diets, more so with high cholecalciferol intakes. However, Ca did not influence 1,25-dihydroxycholecalciferol levels in plasma.

Animals↗
PubMed1979

Intestinal absorption of cholecalciferol in alcoholic liver disease and primary biliary cirrhosis.

The intestinal absorption of (3H)cholecalciferol was studied in five patients with alcoholic liver disease, six patients with primary biliary cirrhosis, and 15 healthy subjects. The rate of appearance in plasma of (3H)cholecalciferol after oral ingestion and the subsequent appearance of (3H) polar metabolites in the alcoholic subjects were similar to those in the healthy subjects. In subjects with primary biliary cirrhosis the rate of appearance in plasma of (3H)cholecalciferol was significantly reduced. The rate of appearance of labelled polar metabolites of cholecalciferol was also lower in this group, suggesting that increased removal of labelled vitamin by conversion into more polar metabolites could not account for the reduced plasma (3H)cholecalciferol response. It is suggested that intestinal absorption of cholecalciferol is usually normal in alcoholic liver disease but impaired in primary biliary cirrhosis. Hepatic 25-hydroxylation is normal in alcoholic liver disease but may be defective in primary biliary cirrhosis.

Adult↗
PubMed1999

Effect of cholecalciferol treatment on the relaxant responses of spontaneously hypertensive rat arteries to acetylcholine.

We studied the effect of oral cholecalciferol treatment on the endothelium-dependent vascular relaxation and hyperpolarization induced by acetylcholine (ACh), which is impaired in spontaneously hypertensive rats (SHR). Adult female SHR and normotensive Wistar-Kyoto rat (WKY) controls received 125 microg of cholecalciferol per kilogram body weight per day for 6 weeks. The responses to ACh of the isolated mesenteric vascular bed and mesenteric artery rings were measured, as well as the smooth muscle cell membrane potential. After cholecalciferol treatment, the systolic blood pressure and basal perfusion pressure of the mesenteric vascular bed of the SHR fell to control levels. The relaxant and hyperpolarizing effects of ACh, which are reduced in SHR, were also brought to control levels after cholecalciferol treatment. These effects of ACh were inhibited by N(omega)-nitro-L-arginine in SHR and by apamin in WKY. After cholecalciferol treatment, SHR hyperpolarizing responses showed the same inhibition pattern as those of WKY. This indicates that, after cholecalciferol treatment, SHR vascular mesenteric preparation responses to ACh are mediated by endothelium-derived hyperpolarizing factor, which induces activation of Ca(2+)-dependent K(+) channels, as in WKY. In untreated SHR, the ACh-mediated response is entirely due to ACh acting via the release of nitric oxide.

Acetylcholine↗
PubMed1981

Stability of an extemporaneous formulation of injectable cholecalciferol.

THe stability of an extemporaneous formulation of injectable cholecalciferol 40,000 IU/ml was assessed. A preparation of cholecalciferol 40,000 IU/ml in a solution of propylene glycol with ethanol 10% was prepared. The solution was stored at 4 degrees C in 2-ml sterile glass vials protected from light. Cholecalciferol content was measured initially and periodically for 199 days using a high-pressure liquid chromatography technique. A 7.3% loss of cholecalciferol potency from baseline was observed over the 199-day period. In contrast to currently available preparations, this extemporaneous formulation of injectable cholecalciferol potentially offers a versatile dosage form for therapeutic or prophylactic therapy of vitamin D deficiency. It was easily prepared and retained more than 90% potency of cholecalciferol for at least six months. The addition of this formulation to large-volume parenteral or parenteral nutrition solutions is not recommended, however, because compatibility data are not available. In addition, the biological activity of the preparation has not been assessed.

Cholecalciferol↗
PubMed1982

Metabolism of cholecalciferol in vitamin D intoxicated chicks.

Vitamin D intoxication was induced in chicks by treatment with large amounts of radioactive cholecalciferol (vitamin D3) either by s.c. injections or by stomach tube. Hypercalcemia and nephrocalcinosis were present, confirming toxicity. The distribution of cholecalciferol and its metabolites in the tissues of the intoxicated birds was compared with that in birds that were treated with physiological amounts of radioactive cholecalciferol. Treatment with pharmacological doses resulted in marked elevation of cholecalciferol and its metabolites in all tissues examined, including elevation of 1 alpha,25-dihydroxycholecalciferol in the intestine. The predominant form of cholecalciferol in these birds was found to be the unchanged vitamin, whereas in birds treated with physiological doses 25-hydroxycholecalciferol was the predominant metabolite. The route of vitamin administration was found to be of importance only when pharmacological doses were given: generally, higher levels were noted when administered via s.c. injections than via stomach tube, except in the arteries. It is suggested that in vitamin D intoxication, the factor responsible for the pathological changes in soft tissues is cholecalciferol itself. High levels of 1 alpha,25-dihydroxycholecalciferol may be responsible for the hypercalcemia.

Animals↗
PubMed1989

Dietary boron modified the effects of magnesium and molybdenum on mineral metabolism in the cholecalciferol-deficient chick.

The metabolic effects of dietary boron, magnesium, and molybdenum on mineral metabolism in the cholecalciferol-deficient chick, with emphasis on growth cartilage histology, were studied. One-day-old cockerel chicks were assigned to groups in a fully-crossed, three factor, 2 x 2 x 2 design. The basal diet was based on ground corn, high-protein casein, and corn oil and contained 125 IU cholecalciferol (inadequate), 0.465 mg B, 2.500 mg Mg, and 0.420 mg Mo/kg. The treatments were the supplementation of the basal diet with B at O or 3; Mg at 300 (inadequate) or 500 (adequate); and Mo at 0 or 20 mg/kg. At d 25, B depressed mortality, alleviated the cholecalciferol-deficiency induced distortion of the marrow sprouts (MS) of the proximal tibial epiphysial plate, and elevated the numbers of osteoclasts within the MS. Adequate Mg exacerbated the cholecalciferol-deficiency induced bone lesions. Mo widened the MS markedly. In Mg-deficient chicks, B elevated plasma Ca and Mg concentrations and growth, but inhibited initiation of cartilage calcification; B had the opposite effect in Mg-adequate chicks. An interaction among B, Mg, and Mo affected plasma uric acid and glucose concentrations. B may function to modify mineral metabolism in cholecalciferol deficiency, suppressing bone anabolism in concurrent Mg deficiency and bone catabolism in concurrent Mg adequacy.

Animals↗
PubMed1969

Metabolism of vitamin D. A new cholecalciferol metabolite, involving loss of hydrogen at C-1, in chick intestinal nuclei.

1. A comparison was made of the nature and intestinal intracellular distribution of the metabolites formed in vitamin D-deficient chicks from [4-(14)C]cholecalciferol and [1-(3)H]cholecalciferol. 2. The simultaneous administration of the two radioactive substances showed the presence in blood, liver, intestine, kidney and bone of cholecalciferol, its ester, 25-hydroxycholecalciferol and a further metabolite of cholecalciferol more polar than 25-hydroxycholecalciferol. The (3)H/(14)C ratios in these four radioactive components were the same as that of the dosed material (4.7:1) with the exception of the most polar material. The (3)H/(14)C ratio was lower in the fourth, most polar, metabolite (0.4:1-1.8:1) in all tissues examined, with the exception of blood. 3. In the chick intestine the polar metabolite accounted for almost 70% of the radioactivity in this tissue after a dose of 0.5mug. of [4-(14)C,1-(3)H]cholecalciferol. This polar metabolite from the intestine also had the lowest (3)H/(14)C ratio of all the tissues. It appears that in the chick intestine the polar metabolite reaches a maximum concentration of 1ng./g. of tissue, above which it cannot be increased irrespective of the dose of the vitamin. 4. The intestinal intracellular organelle with the highest concentration of (14)C radioactivity is the nucleus, and this radioactivity is almost entirely due to the polar metabolite with the lowered (3)H/(14)C ratio, in this case <0.2:1. It appears to be further localized in the chromatin of the nuclei. However, about half of the polar metabolite in the intestine is extranuclear. 5. Double-labelled 25-hydroxycholecalciferol was prepared and after its administration to vitamin D-deficient chicks the polar metabolite with the lowered (3)H/(14)C ratio was detected in liver, kidney, intestine, bone, muscle and heart. 6. None of the polar metabolite with the lowered (3)H/(14)C ratio was detected 16hr. after dosing with either the double-labelled vitamin or the double-labelled 25-hydroxycholecalciferol in blood and adipose tissue of vitamin D-deficient chicks, nor in the intestine, liver and kidney of supplemented birds. 7. The reasons for this loss of (3)H relative to (14)C are discussed in relation to possible chemical structures of this new polar metabolite.

Animals↗
PubMed1973

The transporting proteins of cholecalciferol and 25-hydroxycholecalciferol in serum of chicks and other species. Partial purification and characterization of the chick proteins.

Chick serum contains two cholecalciferol-binding proteins, one of which binds mainly cholecalciferol (cholecalciferol-binding protein) and the other binds 25-hydroxycholecalciferol (25-hydroxycholecalciferol-binding protein). By means of Cohn fractionation, (NH(4))(2)SO(4) precipitation, gel filtration on Sephadex G-200, ion-exchange chromatography on DEAE-Sephadex and an additional gel-filtration step on Sephadex G-100, these two binding proteins were purified. Both proteins possess beta-globulin mobility on analytical polyacrylamide-disc-gel electrophoresis, a sedimentation coefficient of 3.5S and approximate molecular weights of 60000 for the cholecalciferol-binding protein and 54000 for the 25-hydroxycholecalciferol-binding protein. Sera obtained from rat, pig, human and monkey were shown to contain a single binding protein that is responsible for the transport of both cholecalciferol and 25-hydroxycholecalciferol. In the toad the lipoproteins are used for the transport of these two steroids.

Ammonium Sulfate↗
PubMed1979

Metabolism of cholecalciferol in land snails.

1. Radioactively labelled cholecalciferol was injected into the land snails Levantina hiersolyma and Theba pisana. Three metabolites (C, D and E), more polar than cholecalciferol, were found. 2. Metabolite C was found to be identical with 25-hydroxycholecalciferol. On injection of 25-hydroxy[26,27-3H]cholecalciferol, metabolite E was predominantly formed. Metabolite D was predominantly formed from cholecalciferol. Metabolites D and E differ from any known cholecalciferol metabolites. 3. The intestine was found to be the tissue capable of carrying out the transformation of 25-hydroxycholecalciferol into metabolite E. 4. 25-Hydroxycholecalciferol and metabolite E were localized in the digestive gland of the snail, the tissue responsible for the absorption of Ca2+ and its storage. Metabolite D was not localized in any specific tissue.

Animals↗
PubMed1995

Effects of intestinal resection, cholecalciferol and ascorbic acid on iron metabolism in rats.

The effect of dietary supplementation with ascorbic acid or cholecalciferol on Fe utilization was studied using the metabolic balance technique, in rats in which 50% of the distal small intestine was removed, or in which the mid small intestine was transected and reanastomosed (controls). Three different diets were used. The first (basal diet) contained (g/kg dry wt): protein (casein + 50 mg D,L-methionine/g) 120 and fat (medium-chain triacylglycerols, olive oil and sunflower oil, in equal parts) 40. The other diets were obtained by adding ascorbic acid (150 mg/kg diet) or cholecalciferol (0.4 mg/kg diet) to the basal diet. Apparent digestibility coefficient (ADC) and Fe retention were significantly lower in resected animals than in their respective control groups (transected rats). However, the addition of ascorbic acid or cholecalciferol to the basal diet increased the ADC and Fe retention in both transected and resected rats. Five weeks after surgery, resection also resulted in a reduced concentration of Fe in the sternum, but did not reduce the concentration of haemoglobin or serum Fe total Fe-binding capacity or the concentration of Fe in liver, testes, femur or muscle (longissimus dorsi). Supplementation with ascorbic acid increased serum Fe concentration, while the concentration of Fe in muscle was reduced by supplementation with both ascorbic acid and cholecalciferol. Neither supplementation had any effect on the Fe concentration in other tissues, on haemoglobin concentration or plasma total Fe-binding capacity. Thus, supplementation with ascorbic acid or with cholecalciferol increased Fe absorption and reduced the concentration of Fe in muscle.

Animals↗
PubMed1987

Intestinal absorption of cholecalciferol and 25-hydroxycholecalciferol in chronic cholestatic liver disease.

We compared the absorption of cholecalciferol and 25-hydroxycholecalciferol in normal subjects and in patients with mild and severe cholestatic liver disease. 3H-cholecalciferol and 3H-25-hydroxycholecalciferol were given orally and serial blood samples were drawn for measurement of the serum level of radiolabeled vitamin. Absorption of 25-hydroxycholecalciferol peaked earlier and was greater than absorption of cholecalciferol at all times in all three groups. Patients with mild cholestasis (normal bilirubin and fecal fat excretion) absorbed both forms of the vitamin normally. Those with severe cholestasis (jaundice and steatorrhea) had minimal absorption of cholecalciferol but relatively preserved absorption of 25-hydroxycholecalciferol. Absorption of cholecalciferol and 25-hydroxycholecalciferol was inversely related to fecal fat excretion. The superior absorption of 25-hydroxycholecalciferol may partly explain its greater efficacy in oral treatment of vitamin D deficiency in patients with severe cholestasis.

Adult↗
PubMed1991

Intestinal absorption of cholecalciferol and 25-hydroxycholecalciferol in patients with both Crohn's disease and intestinal resection.

We compared the intestinal absorption of cholecalciferol and 25-hydroxycholecalciferol in patients with Crohn's disease and resections of the small bowel. Patients were subgrouped into those with small (less than 100 cm), intermediate (100-300 cm), and large (greater than 300 cm) resections. [3H]cholecalciferol or [3H]25-hydroxycholecalciferol were given orally and serial blood samples were taken for measurement of plasma radiolabeled vitamin. Absorption of both forms of the vitamin decreased with extent of resection but 25-hydroxycholecalciferol absorption was always greater than that of cholecalciferol. When compared with normal control subjects, 25-hydroxycholecalciferol absorption in these patients was better maintained than that of cholecalciferol. These data indicate that vitamin D malabsorption reflects the extent of distal small-bowel resection in Crohn's disease. Treatment with oral cholecalciferol is sufficient in those with small or moderate resections but oral 25-hydroxycholecalciferol supplementation may be preferred in those with a severe short-bowel syndrome.

Absorption↗
PubMed1977

Changes in plasma 25-hydroxycholecalciferol and selected blood parameters after injection of massive doses of cholecalciferol or 25-hydroxycholecalciferol in non-lactating dairy cows.

Plasma levels of 25-hydroxycholecalciferol, free hydroxyproline, calcium, phosphorus, and magnesium were determined in non-lactating, pregnant dairy cows injected intra-muscularly with 15 X 10(6) IU of cholecalciferol or 25 mg of 25-hydroxycholecalciferol. A lag in the conversion of cholecalciferol to 25-hydroxycholecalciferol was observed in the cows injected with cholecalciferol, while an immediate increase was observed when cows were injected with 25-hydroxycholecalciferol directly. The increased plasma levels of 25-hydroxycholecalciferol following injection of cholecalciferol were directly related to rises in plasma free hydroxy-proline, calcium, and phosphorus, while plasma magnesium was inversely related to plasma 25-hydroxycholecalciferol. Injection of 25-hydroxycholecalciferol caused an immediate increase in plasma calcium which persisted for the duration of the experiment. The biological half-life of 25-hydroxycholecalciferol in the injected cows was found to be 34 days. The data indicate the possibility of a feedback mechanism in which massive doses of cholecalciferol inhibit hydroxylation at the 25ths carbon preventing its conversion to 25-hydroxycholecalciferol until after 8 days post injection. The increase in plasma 25-hydroxycholecalciferol after 8 days resulted in increased bone resorption as indicated by plasma free hydroxyproline.

Animals↗
PubMed1980

Absorption and excretion of cholecalciferol and of 25-hydroxycholecalciferol and metabolites in birds.

The absorption and excretion in vivo of cholecalciferol or 25-hydroxycholecalciferol (25-HCC) were determined in chicks (Gallus domesticus) and turkeys (Meleagris gallopavo). The overall net cholecalciferol or 25-HCC absorption in chicks and cholecalciferol in turkey poults was 66.5 +/- 3.3, 74.9 +/- 3.7 and 83.6 +/- 7.1% of the intake, respectively. The absorption of cholecalciferol or 25-HCC in chicks and turkeys occurred at the upper part of the intestine. 25-HCC, esters and non-polar metabolites of cholecalciferol or 25-HCC, and their polar metabolites, were secreted in the duodenum of chicks and turkeys but were partially reabsorbed at the upper part of the jejunum.

Animals↗
PubMed1982

Cholecalciferol requirements of young turkeys under normal conditions and during recovery from rickets.

Day-old turkeys fed vitamin D-deficient diets became rachitic within 17-24 days. The symptoms included reductions in body weight, plasma calcium and inorganic phosphorus, plasma and intestinal calcium-binding protein (CaBP), plasma 25-hydroxycholecalciferol [25(OH)D3], bone ash, and kidney 25(OH)D3-24-hydroxylase and a rise in kidney 25(OH)D3-1-hydroxylase activity. Supplementation of the diet with 12.5 micrograms cholecalciferol per kilogram was sufficient to promote maximal body weight and normal plasma calcium, Plasma calcium, plasma phosphorus and bone ash. Feeding diets containing 250 or 1250 micrograms cholecalciferol per kilogram resulted in a reduced body weight. An increased in the concentration of plasma 25(OH)D3 with increasing dietary cholecalciferol concentration was observed. Feeding vitamin D-deficient rachitic birds for 4 days a diet containing 50 micrograms cholecalciferol per kilogram restored plasma calcium and phosphorus and bone ash. Body weight remained lower than that of the control for an additional 6-day period. Additional cholecalciferol, 25(OH)D3 or 1 alpha-hydroxycholecalciferol in the diet, intramuscular injection of the vitamin D derivatives, or a high-calcium, high-phosphorus diet did not accelerate the recovery from the rachitic state.

Animals↗
PubMed1971

Vitamin D: A cholecalciferol metabolite highly active in promoting intestinal calcium transport.

A major polar metabolite of cholecalciferol (vitamin D(3)) obtained from chick intestines is over four times as effective as cholecalciferol and over two times as effective as 25-hydroxycholecalciferol in stimulating intestinal calcium transport 24 hours after administration. Following a considerable lag, cholecalciferol and its 25-hydroxy derivative produce a maximum stimulation of the transport response at 24 to 48 hours. The polar intestinal metabolite greatly shortens this lag, stimulating maximum calcium transport by 9 hours. At 9 hours this metabolite is at least 13 times as active as the parent cholecalciferol and as such is a likely candidate for the biologically active form of cholecalciferol in the intestine.

Biological Transport↗
PubMed2001

Chronic ingestion of high concentrations of cholecalciferol in cats.

OBJECTIVE: To determine whether ingestion of 63 times the recommended amount of vitamin D3 (cholecalciferol) results in renal calcification or damage in cats. ANIMALS: 20 four-month-old kittens, 17 queens, and 20 kittens born to these queens. PROCEDURE: 4-month-old kittens and queens were given a purified diet with 846 microg of cholecalciferol/kg of diet (high vitamin D3 diet) or 118 microg of cholecalciferol/kg of diet (control diet) for 18 months. Kittens born to queens were weaned onto the same diet given to dams. RESULTS: There were no apparent adverse effects of the high vitamin D3 diet. Plasma cholecalciferol and 25-hydroxycholecalciferol (25-OHD3) concentrations of queens and 4-month-old kittens given the high vitamin D3 diet significantly increased with time. At 6 months, plasma cholecalciferol concentrations in these kittens and queens were 140.0+/-7.3 nmol/L and 423.6+/-26.6 nmol/L, respectively (10 times initial values). Corresponding 25-OHD3 concentration in queens was 587.5+/-59.4 nmol/L (2.5-fold increase over initial values). At 3 months of age, kittens born to queens given the high vitamin D3 diet had an increase in serum BUN and calcium concentrations and a decrease in RBC and serum total protein, albumin, and hemoglobin concentrations. By 18 months, these kittens had an increase in plasma cholecalciferol (276.0+/-22.2 nmol/L) and 25-OHD3 (1,071.9+/-115.3 nmol/L) concentrations. However, all indices of renal function and the appearance of renal tissue on histologic evaluation were normal. CONCLUSIONS AND CLINICAL RELEVANCE: These results indicate that cats are resistant to cholecalciferol toxicosis when the diet is otherwise complete and balanced.

Animals↗