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PubMed1993

The effect of toxic doses of cholecalciferol (vitamin D3) on the serum zinc levels in rats.

Zinc is a trace element important to bone mineralization as well as, in general, nutrition. It is known that cholecalciferol (vitamin D3) affects bone metabolism. In this study, toxic doses of vitamin D3 were injected subcutaneously (25 micrograms/d) to rats for 5 wk. It caused a significant increase in serum zinc levels (p < 0.02). On the other hand, no significant increase was detected in the other groups. Excessive amounts of vitamin D3 caused bone breakdown and increased the levels of zinc in blood.

Alkaline Phosphatase↗

PubMed1976

Cholecalciferol metabolites binding in porcine parathyroid glands.

We studied the cytoplasmic and nuclear binding of 25-hydroxychole-calciferol and 1alpha,25-dihydroxycholecalciferol inside porcine parathyroid glands. Both sterols bind to cytoplasmic components, but a specific nuclear uptake was demonstrated only for 1alpha,25-dihydroxycholecalciferol. These findings support the hypothesis that mammalian parathyroid glands are a target organ for some cholecalciferol metabolites.

Animals↗

PubMed2004

Different effects of physiologically and pharmacologically increased growth hormone levels on cholecalciferol metabolism at prepubertal age.

The aim of the study was to investigate the influence of physiologically and pharmacologically increased plasma growth hormone (GH) levels on cholecalciferol metabolism at prepubertal age. Three groups of dogs raised on the same diet were studied from weaning till 21 weeks of age, i.e., small breed dogs (n = 7, control group); large breed dogs with 15-fold greater growth rates compared to the control group (n = 8, LB-group); and small breed dogs treated with pharmacological doses of growth hormone (n = 6, GH-group; 0.5IU GH per kg body per day) from 12 to 21 weeks of age. Excess of GH had the expected anabolic effect on growth rate and phosphate sparing. Increased plasma GH levels in the LB- and GH-groups versus the control group were accompanied by (1) greater plasma insulin-like growth factor I (IGF-I) levels, (2) greater plasma 1,25-dihydroxycholecalciferol (1,25(OH)(2)D(3)) levels, and (3) lower plasma 24,25(OH)(2)D(3) levels. In the LB-group, excess of GH favored plasma 1,25(OH)(2)D(3) levels by decreasing the clearance of 1,25(OH)(2)D(3), whereas in the GH-group by increasing the production of 1,25(OH)(2)D(3). The lowered plasma 24,25(OH)(2)D(3) levels in the LB- and GH-groups were likely attributed to a competitive inhibition of the production of 24,25(OH)(2)D(3) by GH and/or IGF-I.

Animals↗

PubMed2003

Dietary 135-fold cholecalciferol supplementation severely disturbs the endochondral ossification in growing dogs.

The effects of excessive non-toxic dietary Vitamin D(3) supplementation on Ca homeostasis with specific effects on endochondral ossification and skeletal remodeling were investigated in a group of growing Great Dane dogs supplemented with cholecalciferol (Vitamin D(3); HVitD) versus a control group (CVitD) (1350 microg versus 11.4 microg Vitamin D(3) per kilogram diet) from 6 to 21 weeks of age. There were no differences between groups in plasma concentrations of total Ca, inorganic phosphate, growth hormone, and insulin-like growth factor I and no signs of Vitamin D(3) intoxication in HVitD. For the duration of the study in HVitD compared to CVitD, plasma levels of parathyroid hormone (PTH) decreased, calcitonin (CT) increased, 25-hydroxycholecalciferol [25(OH)D(3)] increased 30- to 75-fold, 24,25-dihydroxycholecalciferol [24,25(OH)(2)D(3)] increased 12- to 16-fold, and 1,25-dihydroxycholecalciferol [1,25(OH)(2)D(3)] decreased by approximately 40%. The latter was attributed to the two-fold increased metabolic clearance rate in the HVitD versus CVitD accompanied by the absence of the anabolic effect of PTH on the production of 1,25(OH)(2)D(3). Fractional Ca absorption (alpha) did not differ between groups at 8 and 14 weeks of age, whereas at 20 weeks of age alpha increased by only 16.4% in HVitD compared to CVitD. Excessive non-toxic Vitamin D(3) supplementation resulted in decreased bone remodeling and focal enlargement of the growth plate with morphology resembling those induced by administration of CT. Hypercalcitoninemia and the imbalanced relationship between 1,25(OH)(2)D(3) and 24,25(OH)(2)D(3) are potent candidates for the disturbed endochondral ossification.

24,25-Dihydroxyvitamin D 3↗

PubMed1988

Effect of age, gonadectomy and hypophysectomy on mitochondrial hydroxylation of vitamin D3 (cholecalciferol) and of 5 beta-cholestane-3 alpha,7 alpha,12 alpha-triol in female and male rat liver.

In a previous study we found that liver mitochondrial side-chain hydroxylation of vitamin D3 (cholecalciferol) and of 5 beta-cholestane-3 alpha,7 alpha,12 alpha-triol was higher in female than in male rats [Saarem & Pedersen (1987) Biochem. J. 247, 73-78]. The present paper describes the effects of age, gonadectomy and hypophysectomy on these activities. The sex difference became manifest above the age of 7 weeks. Ovariectomy and/or injection of oestradiol valerate had no effect on the hydroxylase activities in adult females. Castration increased, and subsequent testosterone treatment decreased, the hydroxylase activities in adult males. Hypophysectomy had no effect in females, but increased the hydroxylase activities in males. Testosterone treatment had no effect in hypophysectomized females or males. Injection of oestradiol valerate had no effect on the hydroxylase activities in hypophysectomized females. In hypophysectomized males this treatment had no effect on the vitamin D3 25-hydroxylase activity, but decreased the C27-steroid 27-hydroxylase activity in males. Microsomal 1 alpha-hydroxyvitamin D3 25-hydroxylase activity was lower in females than in males in all age groups. Castration or hypophysectomy decreased the activity in male rats. It is concluded that, in adult female rats, the mitochondrial side-chain hydroxylation of vitamin D3 and of 5 beta-cholestane-3 alpha,7 alpha,12 alpha-triol is independent of sex hormones. In males these activities are regulated by influence of sex hormones on the hypophysis, probably by the presence of androgens in the neonatal period. Different effects on the two hydroxylases indicate the presence of at least two different cytochromes P-450 in rat liver mitochondria.

Aging↗

PubMed1993

Cholecalciferol supplementation alters gut function and improves digestibility in an underground inhabitant, the naked mole rat (Heterocephalus glaber), when fed on a carrot diet.

Naked mole rats (Heterocephalus glaber) lead a strictly subterranean existence and appear to be naturally deficient in cholecalciferol (D3). Oral supplementation with D3 (Ds) led to a 1.8-fold increase in food intake and the associated enlargement (1.4-fold) of the caecum. The effect of Ds, and the concomitant increase in food intake, on caecal fermentation efficiency when animals were fed on a carrot-based diet was determined by measuring the rate of both gas production and short-chain fatty acid (SCFA) production. Microbial-controlled fermentation processes in the caecum were enhanced with Ds when compared with animals not receiving a D3 supplement (Dn). Both the rates of gas production (Dn 10.76 (SE 0.77), Ds 15.20 (SE 1.77) ml/g dry matter (DM) per h) and SCFA production (Dn 463.0 (SE 33.7), Ds 684.3 (SE 74.8) mumol/g DM per h) increased more than 1.4-fold per g DM caecal substrate. These factors contributed to the higher digestibility of the food in Ds animals. The larger quantity of energy available to D3-replete naked mole rats was not used in anabolic processes, for these animals maintained mass. These findings suggest that metabolic rate in D3-replete animals was elevated. Thus, despite improved gut function, D3-replete animals may be disadvantaged by their higher energy and food requirements in their natural milieu.

Animals↗

PubMed2005

Effects of dietary boron supplementation on some biochemical parameters, peripheral blood lymphocytes, splenic plasma cells and bone characteristics of broiler chicks given diets with adequate or inadequate cholecalciferol (vitamin D3) content.

(1) The effects of 5 and 25 mg/kg boron supplementation of diets with inadequate (6.25 microg/kg) or adequate (50 microg/kg) cholecalciferol (vitamin D3) content on some biochemical parameters, tibia characteristics, peripheral blood lymphocyte and splenic plasma cell counts of broilers were investigated. (2) Supplementation of the diet with boron affected plasma concentrations of boron, iron, copper and zinc and also tibia boron, zinc and calcium concentrations but did not have any effect on tibia iron or copper concentrations or tibia ash and tibia weight values. (3) Boron supplementation caused significant increases in splenic plasma cell count but decreased the proximal and distal tibia growth plate widths. There was no effect of boron supplementation on peripheral blood alpha-naphthyl acetate esterase (ANAE) content. Whole blood haematocrit and haemoglobin counts were significantly increased by boron supplementation but there were no effects on leucocyte ratios such as eosinophil, basophil, monocyte, lymphocyte and thrombocyte. (4) In general, the findings of the present study support the hypothesis that boron has an important biological role that affects the mineral metabolism of animals by influencing both biochemical and haematological mechanisms.

Albumins↗

PubMed1988

Effects of cholecalciferol or calcium deficiency on oestrogen metabolism in the laying hen.

1. Seventeen 32-week-old White Leghorn laying hens were induced to become deficient in calciferol or in calcium (laying thin or soft shelled eggs) by withdrawing either cholecalciferol (27.5 micrograms/kg diet) or calcium (31 g/kg diet) supplements from the control diet. 2. The metabolic fate and metabolic clearance rate (MCR) of intravenously injected 3H-oestradiol-17 beta were then monitored for 40 min. 3. In both the calciferol and calcium-deficient groups a major oestrogen sulphate pathway was particularly affected, resulting in a decreased conversion of oestradiol-17 beta-3-sulphate to oestradiol-17 alpha-3-sulphate, with a concomitant reduced MCR of oestradiol-17 beta from plasma. 4. The metabolic defect was corrected by feeding the control diet. 5. Because the metabolic defect observed in calciferol deficiency occurred in Ca deficiency in a more severe form, we conclude that the more immediate cause was calcium rather than calciferol deficiency. To our knowledge, this is the first observation of a calcium-deficient effect on oestrogen sulphate metabolism in vivo.

Animals↗

PubMed1993

Effect of dietary contents of cholecalciferol, 1 alpha,25-dihydroxycholecalciferol and 24,25-dihydroxycholecalciferol on blood concentrations of 25-hydroxycholecalciferol, 1 alpha,25-dihydroxycholecalciferol, total calcium and eggshell quality.

1. Withdrawal of cholecalciferol (D3) supplement from a layers diet drastically reduced blood 25-hydroxycholecalciferol (25-OH-D3), 1 alpha,25-dihydroxycholecalciferol (calcitriol) and egg specific gravity (SG) within two weeks, followed by a decrease in blood total calcium (Ca). 2. Doubling the D3 supplement in the control diet (27.5 micrograms or 1100 IU/kg) almost linearly increased the circulating concentration of 25-OH-D3 without raising the concentration of calcitriol, Ca, or egg SG. 3. Replacing D3 by the optimal concentration of calcitriol (5 micrograms/kg diet) improved egg SG after 21 weeks of treatment without increasing blood calcitriol or total Ca. 4. By itself, 24,25-dihydroxycholecalciferol [24,25-(OH)2D3] was unable to maintain normal blood levels of calcitriol, Ca or egg SG and, when added together with calcitriol in the diet, tended to elevate blood Ca but suppress the beneficial effect of calcitriol on shell quality, with little or no effect on blood calcitriol.

24,25-Dihydroxyvitamin D 3↗

PubMed1993

Effect of dietary vitamin D3 (cholecalciferol) on colon carcinogenesis induced by 1,2-dimethylhydrazine in male Fischer 344 rats.

This study examined the effect of increasing dietary vitamin D on chemically induced colon carcinogenesis. Male Fischer 344 rats were first injected with 1,2-dimethylhydrazine (200 mg/kg) and then fed one of five dietary levels of vitamin D as cholecalciferol (250, 1,000, 2,000, 4,000, and 10,000 IU/kg diet) for nine months. Dietary vitamin D3 had no effect on weight gain. Plasma 25-hydroxyvitamin D3 levels were similar for the 1,000 and 2,000 IU/kg groups but varied in a dose-related manner for the other groups. Vitamin D did not significantly alter the tumor incidence in either the distal or the proximal colon. No significant differences in the labeling index were found in either the proximal or the distal colon. Within the distal colon, the proliferative zone increased in a dose-related manner. Distribution of labeled cells within the crypt compartments was not affected by dietary vitamin D. Bone and serum minerals in general were unaffected by dietary vitamin D. This study shows that, at this level of dietary calcium, vitamin D did not affect 1,2-dimethylhydrazine-induced colon carcinogenesis.

1,2-Dimethylhydrazine↗

PubMed1994

Single-dose cholecalciferol suppresses the winter increase in parathyroid hormone concentrations in healthy older men and women: a randomized trial.

A randomized double-blind controlled trial of a single oral dose of 2.5 mg (100,000 IU) cholecalciferol (vitamin D3) was conducted in the winter in 189 healthy free-living men and women aged 63-76 y. The mean baseline serum concentration for 25-hydroxyvitamin D was 34.5 nmol/L and for parathyroid hormone 3.18 pmol/L. After 5 wk, mean serum 25-hydroxyvitamin D concentrations were 60% higher in the treated than in the placebo group (P < 0.001). There was a 12% difference in parathyroid hormone concentrations in the treated compared with the placebo group (P < 0.001). No differences in serum calcium were seen. Findings suggest that 25-hydroxyvitamin D has a physiological role in the regulation of parathyroid secretion independent of serum calcium in healthy elderly people. Parathyroid concentrations rise and 25-hydroxyvitamin D concentrations decline with age. These results may have implications for the prevention of osteoporotic fractures that occur with increased frequency in winter and in elderly people.

Aged↗

PubMed1977

Relative activities of some metabolites and analogs of cholecalciferol in stimulation of tibia ash weight in chicks otherwise deprived of vitamin D.

Nine metabolites and analogs of cholecalciferol (CC) were tested for ability to increase tibia ash weight in chicks otherwise deprived of vitamin D. All of the compounds promoted bone mineralization in a linear log dose-response relationship. The maximal response obtained for any compound was an approximate doubling in bone ash weight compared to vehicle-treated controls. Relative potencies, based upon the calculated ash weight doubling dose, were as follows: 1 alpha, 25-(OH)2-CC = 1 alpha-OH-CC greater than CC greater than 25-OH-CC greater than 24R, 25-(OH)2-CC = 1 alpha,24R, 25-(OH)3- CC greater than 5,6-trans-25-OH-CC greater than 1 alpha, 24S, 25- (OH)3-CC greater than 5,6-trans-CC greater than 24S, 25-(OH)2-CC.

Animals↗

PubMed1977

Relative toxicity and metabolic effects of cholecalciferol and 25-hydroxycholecalciferol in chicks.

The relative toxicity and metabolic effectiveness of cholecalciferol (CC) and 25-hydroxycholecalciferol (25-HCC) in chicks were evaluated by feeding six graded levels of each and observing gross and microscopic pathology as well as several metabolic parameters of calcium metabolism. Renal tubular calcification was observed when CC was fed at the rate of 10.0 mg/kg of diet and when 25-HCC was fed at the rate of 0.1 mg/kg diet. Thus, 100-fold increase in toxicity results when the hydroxylated form of CC is fed. Both microscopic renal lesions and increased renal calcium and inorganic phosphate concentrations occurred in chicks with normal serum calcium concentrations.

Alkaline Phosphatase↗

PubMed1982

Relative biopotency of dietary ergocalciferol and cholecalciferol and the role of and requirement for vitamin D in rainbow trout (Salmo gairdneri).

A growth assay was conducted for six consecutive 28-day periods by using triplicate groups of 110 rainbow trout with an average initial body weight of 3.0 g. Ergocalciferol (vitamin D2 or D2) and cholecalciferol (vitamin D3 or D3) were included to provide levels of 200, 400 and 800 iu/kg in a semipurified casein, gelatin diet. Further treatments with 0 vitamin D and 1600 IU/kg of D3 were also included. The resulting growth curves were significant for parallelism. Statistical analysis showed that D3 was 3.27 times as potent as D2 (limits 2.33 to 4.58). The dietary requirement for D3 was found to be in excess of 800 iu/kg of diet. Vitamin D-deficient fish showed no change in bone ash but exhibited clinical manifestations of tetany with no hypocalcemia. A complete absence of tetany was seen only in the groups fed 800 and 1600 IU of D3 per kilogram. None of the levels of D2 used were sufficient to completely alleviate symptoms of this disorder. These studies of rainbow trout provide evidence that vitamin D is required for the normal functioning of white muscle without altering the calcium content of the plasma or epaxial musculature.

Animals↗

PubMed1982

Disorders of cholecalciferol metabolism in old egg-laying hens.

It has been reported that the rate of cracked or soft-shelled eggs markedly increases in old laying hens. We investigated the effect of age on cholecalciferol metabolism in different age groups of laying hens. The egg production rate in hens more than 500 days old was maintained within a range of about 70% of that in young hens (230-320 days old), whereas the rate of cracked or soft-shelled eggs increased markedly with age. When kidney homogenates from the different age groups were incubated with [3H]-25-hydroxyvitamin D-3, renal 25-hydroxyvitamin D-3-1 alpha-hydroxylase activity was found to decrease markedly with age. When birds were given intravenously either [3H]-25-hydroxyvitamin D-3 or [3H]-1 alpha,25-dihydroxyvitamin D-3, the accumulation of [3H]-1 alpha,25-dihydroxyvitamin D-3 in plasma and target tissue also decreased with age. Forced molting performed in old hens restored eggshell quality. The treatment also restored, though partially, the in vivo accumulation of [3H]-l alpha,25-dihydroxyvitamin D-3 in the target tissues. These results suggest that the increased rate of cracked or soft-shelled eggs seen in older birds is associated with disorders of vitamin D-3 metabolism.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗

PubMed1988

Egg shell quality and cholecalciferol metabolism in aged laying hens.

Calcium-binding protein D28K (calbindin) synthesis, vitamin D metabolism and shell quality were investigated in young and aged laying hens fed diets containing either cholecalciferol (CC) or its 1-hydroxylated derivatives. Duodenal calbindin concentration was similar in the young and in the aged laying hens. Exogenous 1-hydroxylated CC derivatives increased duodenal calbindin concentration, regardless of age. Shell weight and shell density (mg/cm2) were significantly lower (P less than 0.01) in the aged than in the young hens. Egg shell weight and density tended to decrease along the clutch. The rate of decline was higher in aged than in young hens. Feeding aged hens a diet containing 5 micrograms 1,25-dihydroxycholecalciferol [1,25(OH)2CC] or 1 alpha-hydroxycholecalciferol per kilogram improved shell quality, slowed down the progressive reduction in shell quality during the clutch and increased culling and mortality. The results indicate a) that the capacity for expression of 1,25(OH)2D3 in the intestine is not altered by age and b) that prolonged feeding of 1-hydroxylated derivatives of vitamin D3 improves shell quality in aged laying hens and increases culling and mortality.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗

PubMed1989

The effect of dietary cholecalciferol, 25-hydroxycholecalciferol and 1,25-dihydroxycholecalciferol on the development of tibial dyschondroplasia in broiler chickens in the absence and presence of disulfiram.

Four experiments were conducted to determine the effect of dietary cholecalciferol (vitamin D3), 25-hydroxycholecalciferol (25-OHD3) and 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) on the changes in growth, feed efficiency and bone ash, and the incidence, severity and number of #3 scores of tibial dyschondroplasia caused by the addition of disulfiram to the diet. The basal diet used was low in calcium and high in phosphorus and chlorine and known to promote a high incidence of tibial dyschondroplasia in broiler chickens. The chickens in all experiments received enough ultraviolet radiation from fluorescent lights in the pens to nearly satisfy their need for vitamin D. The addition of disulfiram to the diet caused an increase in most of the measurements indicating development of tibial dyschondroplasia in all of the experiments, and caused a decrease in bone ash in two of the experiments and a decrease in growth and gain:feed in one experiment. The addition of D3 to a diet containing no D3 caused higher bone ash and lower incidence of tibial dyschondroplasia in the absence or presence of disulfiram. The effects of the addition of 25-OHD3 to diets containing approximately five times the requirement of D3 in the absence and presence of disulfiram caused variable results. The addition of 1,25-(OH)2D3 to the D3-supplemented diet in the absence or presence of disulfiram caused dramatic increases in bone ash and a decrease in most of the criteria used to measure development of tibial dyschondroplasia. There was no indication of interaction of the effects of D3, 25-OHD3 and 1,25-(OH)2D3 with the action of disulfiram.

Animals↗

PubMed1999

Plasma 25-hydroxyvitamin D in growing kittens is related to dietary intake of cholecalciferol.

Vitamin D synthesis by growing kittens exposed to ultraviolet light is ineffective. Concentration of 25-hydroxyvitamin D (25-OHD) in plasma (the most useful index of vitamin D status) was measured in six groups each of seven kittens given a purified diet (12 g calcium and 8 g phosphorus/kg, calculated metabolizable energy = 20 kJ/g) that contained either 0.0, 3.125, 6.25, 12.5, 18.75 or 25 microg of cholecalciferol/kg diet. All kittens received these diets from 9 to 22 wk of age, and the two groups given the 0.0 and 3.125 microg cholecalciferol/kg treatments continued to receive the diets until they were 34 wk old. Total and ionizable calcium and phosphorus in plasma were not affected by treatments. No adverse clinical changes were observed or found on radiographic examination of the kittens at 22 or 34 wk of age. Plasma concentration of 25-OHD was linearly related (r2 = 0.99, P < 0.001) to dietary intake of cholecalciferol. Plasma concentration of 25-OHD in kittens given the diet without added vitamin D was significantly less at 22 wk than at 9 wk, whereas kittens receiving the diet containing 3.125 microg cholecalciferol/kg had significantly higher 25-OHD concentrations at 22 and 34 wk than at 9 wk of age. Kittens given the 6.25 microg cholecalciferol/kg diet had plasma 25-OHD concentrations at 22 wk > 50 nmol/L which is considered replete for humans. An allowance of 6. 25 microg (250 IU) of cholecalciferol/kg diet is suggested to provide a margin of safety.

25-Hydroxyvitamin D 2↗