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PubMed2000

Improved cholecalciferol nutrition in rats is noncalcemic, suppresses parathyroid hormone and increases responsiveness to 1, 25-dihydroxycholecalciferol.

We examined how cholecalciferol (vitamin D) nutrition affected serum 25-hydroxycholecalciferol (25(OH)D) and 1, 25-dihydroxycholecalciferol (1,25(OH)(2)D). Rats were fed conventional diet (vitamin D, 4.5 IU/g, or 7 nmol/d) or the same diet plus 18 nmol/d of extra vitamin D for 3 wk. The extra vitamin D resulted in greater serum 25(OH)D (51 +/- 3, vs. control of 21 +/- 2 nmol/L), and kidney mRNA for vitamin D receptor [VDR mRNA] (P = 0. 026) and lower serum 1,25(OH)(2)D (72 +/- 16 vs. control of 161 +/- 10 pmol/L, P = 0.001), and parathyroid hormone (PTH) (89 +/- 4 vs. control of 160 +/- 15 ng/L, P = 0.001). Kidney VDR mRNA relative to GAPDH mRNA correlated inversely with serum 1,25(OH)(2)D (r = -0.714, P = 0.006). There were no differences in serum calcium, phosphate, alkaline phosphatase, or weight gain. Experiment 2 compared groups supplemented with 0.2, 2 or 20 nmol/d of vitamin D orally, or 20 nmol/d dermally to see how vitamin D nutrition influenced the response of 1,25(OH)(2)D to changes in diet calcium. Vitamin D did not affect urinary calcium or pyridinoline excretion, serum calcium, phosphate, vitamin D binding protein or alkaline phosphatase. In groups given 20 nmol/d of vitamin D, renal mitochondrial 25(OH)D-1alpha-hydroxylase was lower (P < 0.01) and 25(OH)D-24-hydroxylase was higher (P < 0.05). Higher 25(OH)D concentration was related to proportionally lower 1,25(OH)(2)D at every calcium intake, indicating greater tissue sensitivity to 1, 25(OH)(2)D. We conclude suppression of 1,25(OH)(2)D and PTH, and higher renal VDR mRNA and 24-hydroxylase did not involve higher free 1,25(OH)(2)D concentration or a first pass effect at the gut. Thus, 25(OH)D or a metabolite other than 1,25(OH)(2)D is a physiological, transcriptionally and biochemically active, noncalcemic vitamin D metabolite.

Animals↗

PubMed2002

Moderate cholecalciferol supplementation depresses intestinal calcium absorption in growing dogs.

Hormonal regulation of calcium (Ca) absorption was investigated in a cholecalciferol (vitamin D(3))-supplemented group (hVitD) vs. a control group (cVitD) of growing Great Danes (100 vs. 12.5 micro g vitamin D(3)/kg diet). Although Ca intakes did not differ, fractional Ca absorption was significantly lower in the hVitD group than in the cVitD group. There were no differences in plasma concentrations of Ca, inorganic phosphate, parathyroid hormone, growth hormone or insulin-like growth factor I between groups. Plasma 25-hydroxycholecalciferol [25(OH)D(3)] concentrations were maintained in the hVitD dogs at the same levels as in the cVitD dogs due to increased turnover of 25(OH)D(3) into 24,25-dihydroxycholecalciferol [24,25(OH)(2)D(3)] and 1,25-dihydroxycholecalciferol [1,25(OH)(2)D(3)]. In hVitD dogs, the greater plasma 24,25(OH)(2)D(3) concentration and the enhanced metabolic clearance rate (MCR) of 1,25(OH)(2)D(3) indicated upregulated 24-hydroxylase activity. The increased MCR of 1,25(OH)(2)D(3) decreased plasma 1,25(OH)(2)D(3) concentrations. In hVitD dogs, the greater production rate of 1,25(OH)(2)D(3) was consistent with the 12.9-fold greater renal 1alpha-hydroxylase gene expression compared with cVitD dogs and compensated to a certain extent for the accelerated MCR of 1,25(OH)(2)D(3). The moderately decreased plasma 1,25(OH)(2)D(3) concentration can only partially explain the decreased Ca absorption in the hVitD dogs. Intestinal vitamin D receptor concentrations did not differ between groups and did not account for the decreased Ca absorption. We suggest that 24,25(OH)(2)D(3) may downregulate Ca absorption.

25-Hydroxyvitamin D3 1-alpha-Hydroxylase↗

PubMed1997

Utilization of phytate phosphorus and calcium as influenced by microbial phytase, cholecalciferol, and the calcium: total phosphorus ratio in broiler diets.

The present study was performed to evaluate the potential of microbial phytase and cholecalciferol (D3) for improving the utilization of phytate P and Ca and the influence of the Car:total (t) P ratio in a corn-soybean meal diet fed to broilers from hatch to 21 d of age. A 4 x 4 x 2 factorial arrangement of treatments was used: 1.1, 1.4, 1.7, and 2.0:1 Ca:tP ratio; 0, 300, 600, and 900 U of phytase/kg of diet; and 66 and 660 micrograms of D3/kg of diet. Another four treatments were included: the four Ca:tP ratios with 6,600 micrograms of D3 addition, but without phytase. Added phytase linearly increased (P < 0.001) BW gain, feed intake, toe ash content, and P and Ca retention; these measurements were negatively influenced by widening the dietary Ca:tP ratio, and synergetically improved by addition of D3. Increasing the Ca:tP ratio decreased (P < 0.001) all measurements in the presence or absence of supplemental phytase and D3. Dietary Ca:tP ratios between 1.1:1 to 1.4:1 appears critical to the efficient use of supplemental phytase and D3 for improving the utilization of phytate P and Ca. The addition of D3 in corn-soybean meal diets indicated a potential for improving the utilization of phytate P and Ca by increasing Ca and P retention by about 5 to 12% in birds, which led to an increase in toe ash content (P < 0.03). The enhanced phytate P utilization (P < 0.001) was also observed during assay of the phytase activity in the mixed diets with an addition of D3 and without added phytase. In summary, the findings of this study suggested that phytase, D3, and Ca:tP are important factors in degrading phytate and improving phytate P and Ca utilization in broilers.

6-Phytase↗

PubMed1997

Evidence of increased cholecalciferol requirement in chicks with tibial dyschondroplasia.

A series of experiments was conducted to test the hypothesis that vitamin D utilization may not be as efficient in chicks with tibial dyschondroplasia (TD). The basal diet contained 1.0% Ca and 0.45% available P with no supplemental cholecalciferol (D3). Chicks from low TD (LTD) and high TD (HTD) selected lines were fed diets supplemented with various levels of vitamin D compounds and examined for rickets and TD. When chicks were fed a D3-deficient diet containing only 1.25 micrograms/kg added D3, HTD chicks had a greater incidence of severe rickets than LTD chicks (P < 0.05). The LTD chicks did not exhibit TD when fed a diet containing adequate (20 micrograms/kg) D3. The LTD chicks fed a diet supplemented with 5 micrograms/kg D3, however, had 22% incidence of TD. When HTD chicks were fed diets supplemented with 5 micrograms/kg D3 [control diet that meets NRC (1994) requirement for D3], 20 micrograms/kg D3, 5 micrograms/kg 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] or the combination of both D3 (20 micrograms/kg) and 1,25-(OH)2D3 (5 micrograms/ kg), TD incidence was highest in HTD chicks fed the control diet. When HTD chicks were fed diets with an increased dietary level of 1,25-(OH)2D3 (10 micrograms/kg) further reduction of TD incidence (P < 0.05) occurred. A potentially toxic level (Soares et al., 1983) of 1,25-(OH)2D3 (15 micrograms/kg) fed to HTD chicks resulted in still greater suppression of incidence of TD even though growth and feed intake in HTD chicks was greater than those of LTD chicks. It is concluded that the development of TD in HTD chicks is associated with subnormal ability to metabolize vitamin D.

Animals↗

PubMed1998

The influence of vitamin A on the utilization and amelioration of toxicity of cholecalciferol, 25-hydroxycholecalciferol, and 1,25 dihydroxycholecalciferol in young broiler chickens.

Three experiments were conducted to determine the influence of vitamin A on the utilization and amelioration of toxicity of cholecalciferol (vitamin D3), 25-hydroxycholecalciferol [25-(OH)D3], and 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] in young broiler chicks. Two levels of vitamin A (1,500 and 45,000 IU/kg or 450 and 13,500 microg) were fed in all experiments. In Experiment 1, chicks were fed six levels of vitamin D3 (0, 5, 10, 20, 40, and 80 microg/kg). High dietary vitamin A decreased bone ash (P < 0.001), and increased the incidence of rickets (P < or = 0.02). Linear and quadratic responses to vitamin D3 levels were significant (P < 0.01) for body weight, bone ash, incidence and severity of rickets, and plasma calcium. In Experiment 2, six levels of 25-(OH)D3 (0, 5, 10, 20, 40, and 80 microg/kg) were added to the basal diet. Adding 25-(OH)D3 increased (P < 0.001) body weight, bone ash, and plasma calcium, and decreased rickets and plasma vitamin A. Adding 25-(OH)D3 overcame the reduction in bone ash produced by high dietary vitamin A showing a significant (P < 0.02) interaction. In Experiment 3, six levels of 1,25-(OH)2D3 (0, 2, 4, 8, 16, and 32 microg/kg) were added to the basal diet. High dietary vitamin A increased (P < 0.01) the incidence and severity of rickets. Adding 1,25-(OH)2D3 increased (P < 0.01) body weight, bone ash, plasma calcium, and reduced rickets and plasma and liver vitamin A. Adding 1,25-(OH)2D3 overcame the reduction in bone ash, and the increase in rickets produced by high vitamin A was significant (P < or = 0.05). These results indicate that high dietary vitamin A (45,000 IU/kg) interferes with the utilization of vitamin D3, 25-(OH)D3 and 1,25-(OH)2D3, increasing the requirement for each of them. Moreover, 45,000 IU/kg of dietary vitamin A ameliorated the potential toxic effects of feeding high levels of vitamin D3, 25-(OH)D3 and 1,25-(OH)2D3 to young broiler chickens. Further work is necessary to find the minimum levels of these vitamins needed to cause these effects.

Animals↗

PubMed1998

Effects and interactions of dietary levels of vitamins A and E and cholecalciferol in broiler chickens.

Four experiments were conducted to determine the effects and interactions of feeding different levels of vitamins A, cholecalciferol (vitamin D3), and E on broiler chicks. In Experiment 1, chicks were fed marginal vitamin D3 (500 IU/kg) and increasing dietary levels of vitamin A (5,000, 10,000, 20,000, 40,000, 80,000, and 160,000 IU/kg). Bone ash was reduced by 10,000 IU/kg of vitamin A in the diet and at vitamin A levels above 20,000 IU/kg of diet body weight was reduced. In Experiment 2, two levels of vitamin A (1,500 and 15,000 IU/kg) and six levels of vitamin E (10, 500, 1,000, 2,500, 5,000, and 10,000 IU/kg) were added to the basal diet. High levels of vitamins A and E significantly (P < 0.001) reduced bone ash. The vitamin A x E interaction was significant (P < or = 0.05) for rickets. In Experiment 3, the same two levels of vitamin A as Experiment 2 and six levels of vitamin D3 (500, 1,000, 1,500, 2,000, 2,500, and 3,000 IU/kg) were added to the basal diet that contained 10,000 IU/kg of vitamin E. Body weight and bone ash were increased by increasing vitamin D3 with a corresponding reduction (P < or = 0.05) in rickets. In Experiment 4, three levels of vitamin A (1,500, 15,000, and 45,000 IU/kg), three levels of vitamin D3 (500, 1,500, and 2,500 IU/kg), and three levels of vitamin E (10, 5,000, and 10,000 IU/kg) were added to the basal diet. Significant negative responses (P < or = 0.05) to increasing dietary vitamin A were observed for bone ash, rickets, and plasma and liver vitamin E. A significant (P < 0.001) increase in bone ash and plasma calcium with a corresponding reduction in rickets was observed by increasing vitamin D3. Increasing dietary vitamin E adversely affected (P < or = 0.01) bone ash, plasma calcium, and plasma and liver vitamin A concentrations. These results indicate the need for making feed with the proper ratios of vitamins A, D3, and E.

Animals↗

PubMed2002

Quantitative evaluation of 1-alpha-hydroxycholecalciferol as a cholecalciferol substitute for broilers.

Two experiments were conducted using a corn-soybean meal diet that meets or exceeds the NRC (1984) requirements for all nutrients except cholecalciferol (D3) to determine the effectiveness of 1-alpha-hydroxycholecalciferol (1alpha-OHD3) as a substitute for D3 in the diet of young broilers. Ross x Ross mixed-sex, 1-d-old chicks were reared in Petersime battery brooders not exposed to ultraviolet light with feed and water supplied ad libitum for 16 d. In Experiment 1, D3 was fed at 0, 2.5, 5, 10, 20, and 40 microg/kg and one source of 1alpha-OHD3-(Hoffmann-LaRoche, Inc.; HLR) was fed at 0.625, 1.25, 2.5, 5, and 10 microg/kg of diet. In Experiment 2, the D3 was fed at 0, 2.5, 5, and 10 microg and two sources of 1alpha-OHD3-[HLR and Majestic Research Inc. (MRI)] were fed at 0, 0.625, 1.25, and 5 microg/kg of diet. Slope ratio analysis of data from the measurement of 16-d body weight, plasma Ca, rickets, and bone ash indicated bioavailability of the 1alpha-OHD3 as compared to D3 from 1.88 to 21.2. Percentage bone ash gave the most precise values in both experiments. Considering all the data from both experiments, the 1alpha-OHD3 appears to be approximately eight times as effective as D3 for satisfying the requirements of several criteria in two experiments with broiler chickens.

Animal Feed↗

PubMed2002

Studies on the efficacy of cholecalciferol and derivatives for stimulating phytate utilization in broilers.

Studies were conducted to determine the effect of dietary supplementation with cholecalciferol (D3), 1,25-dihydroxycholecalciferol [1,25-(OH)2D3], 1alpha-hydroxycholecalciferol (1alpha-OHD3), and 25-hydroxycholecalciferol (25-OHD3) on utilization of phytate P by broiler chickens. Three experiments were conducted with corn-soybean meal type diets with D3 and 1,25-(OH)2D3 being tested in one experiment and 1,25-(OH)2D3, 1alpha-OHD3, and 25-OHD3 being tested in two experiments of exactly the same design. In the first experiment, high levels of D3 (110 microg and 220 microg/kg of diet) increased phytate P utilization, but the increase was not as great as that obtained from 1,25-(OH)2D3 supplementation. In the other two experiments, 1,25-(OH)2D3, D3 and 1alpha-OHD3 were consistently effective in increasing phytate P utilization as measured by plasma Ca and P, incidence of P rickets, bone ash, and retention of Ca, P, and phytate P. Supplementation with 25-OHD3 in general gave smaller and more inconsistent responses to these criteria, indicating some inconsistency in its ability to improve phytate P utilization.

Animal Nutritional Physiological Phenomena↗

PubMed2005

Effect of the level of cholecalciferol supplementation of broiler breeder hen diets on the performance and bone abnormalities of the progeny fed diets containing various levels of calcium or 25-hydroxycholecalciferol.

Four experiments were conducted using Ross x Ross chicks hatched from broiler breeder hens fed various levels of cholecalciferol (vitamin D3; 0 to 4,000 IU/kg of diet) to determine the effect of the maternal diet on the performance and leg abnormalities of the progeny. Chicks hatched from eggs laid by the hens at different ages were used in experiments 1 to 4. The studies were conducted in an ultraviolet light-free environment as split plot designs, with Ca levels or 25-hydroxycholecalciferol (25-OHD3) in the chicks' diet as the whole plot, and vitamin D3 in the maternal diet as a subplot. Chicks in experiments 1 and 2 were fed 2 levels of Ca (0.63% or 0.90%) and chicks in experiments 3 and 4 were fed 6 levels of 25-OHD3 (0 to 40 microg/kg of diet). Significant increases in body weight gain (BWG) of the progeny were observed in experiments 1, 2, and 4 as the vitamin D3 level in the maternal diet increased. Chicks hatched from eggs laid by hens fed the highest levels of D3 had the highest tibia ash. Significant reductions in Ca rickets incidence (experiments 1 and 2) and tibial dyschondroplasia (TD) incidence (experiment 1) were observed as the level of vitamin D3 in the maternal diet increased. Chicks fed lower levels of Ca had lower BWG and tibia ash and higher incidences of TD and Ca rickets than chicks fed higher levels of Ca. Increasing the level of 25-OHD3 in the chicks' diet significantly improved BWG, tibia ash, and plasma Ca and reduced TD and Ca rickets incidence. An overall evaluation of the study indicates that chicks from hens fed the highest levels of vitamin D3 and fed high levels of Ca or 25-OHD3 had the highest BWG, tibia ash, and plasma Ca, and the lowest incidences of TD and Ca rickets.

Animal Feed↗

PubMed2005

Twenty-five hydroxycholecalciferol as a cholecalciferol substitute in broiler breeder hen diets and its effect on the performance and general health of the progeny.

An experiment was conducted with broiler breeder hens to determine the relative biological value of 25-hydroxycholecalciferol (25-OHD3) compared with cholecalciferol (vitamin D3) for hen-day egg production, hatchability, embryo mortality (early, 1 to 10 d of incubation, late, 11 to 21 d), and body ash of the progeny. The study was conducted with 73-to-90-wk-old molted Ross broiler breeder hens in an environment excluding ultraviolet light. A basal vitamin D3 deficient diet supplemented with 4 levels of vitamin D3 (0, 3,125, 12,500, and 50,000 ng/kg of diet) and 2 levels of 25-OHD3 (3,125 and 12,500 ng/kg of diet) was fed. The relative biological values of 25-OHD3 in comparison to vitamin D3, using slope ratio techniques, were 138, 133, 128, and 111% for hen-day egg production, hatchability, late embryo mortality, and body ash of the progeny,, respectively (average = 128%). When comparing 25-OHD3 against D3 at the 3,125 ng/kg level, the relative biological values were 209, 167, 400, and 108% for the same criteria, respectively (average = 221%). However, at the 12,500 ng/kg level no statistical differences between 25-OHD3 and D3 were observed (average = 108%). Four trials were conducted to determine the effect of the maternal diet on the performance and leg abnormalities of the hens' progeny. In experiment 1, no vitamin D was added to the corn-soybean meal basal diet fed to the chicks, and in experiments 2, 3, and 4 the basal diet was supplemented with 27.5 microg of D3/kg of diet. In the progeny study, the average relative biological value of 25-OHD3 at the 3,125 and 12,500 ng/kg levels were 115 and 101%, respectively. The potency of 25-OHD3 in relation to vitamin D3 depended on the level tested. When comparing vitamin D sources, 25-OHD3 had greater potency than D3 only at very low levels of supplementation.

Aging↗

PubMed2003

Effect of four monthly oral vitamin D3 (cholecalciferol) supplementation on fractures and mortality in men and women living in the community: randomised double blind controlled trial.

OBJECTIVE: To determine the effect of four monthly vitamin D supplementation on the rate of fractures in men and women aged 65 years and over living in the community. DESIGN: Randomised double blind controlled trial of 100 000 IU oral vitamin D3 (cholecalciferol) supplementation or matching placebo every four months over five years. SETTING AND PARTICIPANTS: 2686 people (2037 men and 649 women) aged 65-85 years living in the general community, recruited from the British doctors register and a general practice register in Suffolk. MAIN OUTCOME MEASURES: Fracture incidence and total mortality by cause. RESULTS: After five years 268 men and women had incident fractures, of whom 147 had fractures in common osteoporotic sites (hip, wrist or forearm, or vertebrae). Relative risks in the vitamin D group compared with the placebo group were 0.78 (95% confidence interval 0.61 to 0.99, P=0.04) for any first fracture and 0.67 (0.48 to 0.93, P=0.02) for first hip, wrist or forearm, or vertebral fracture. 471 participants died. The relative risk for total mortality in the vitamin D group compared with the placebo group was 0.88 (0.74 to 1.06, P=0.18). Findings were consistent in men and women and in doctors and the general practice population. CONCLUSION: Four monthly supplementation with 100 000 IU oral vitamin D may prevent fractures without adverse effects in men and women living in the general community.

Administration, Oral↗

PubMed1980

Influence of cholecalciferol on tissue zinc homeostasis in the rat.

A role for calciferol in zinc homeostasis was investigated by radioisotope uptake and compartmental analysis techniques. cholecalciferol was injected into rats 4-5 days prior to radioisotopic study of rapidly exchangeable pools (< 4 h). Kidney, liver, and duodenum had significant increases in zinc uptake rates. Bone and skeletal muscle had significant decreases. No other tissues had significant differences. Compartmental analysis models generated by the SAAM-25 digital computer program suggested a decrease in the fractional tissue to plasma coefficient to be the mechanism for the observed changes in the serum zinc concentration and tissue zinc accumulation rates. It is not clear whether this is a specific effect of calciferol on zinc homeostasis or is a nonspecific response which may reflect some role for zinc in calciferol metabolism.

Animals↗

PubMed1972

Evidence for a direct action of cholecalciferol and 25-hydroxycholecalciferol on the renal transport of phosphate, sodium, and calcium.

Acute clearance studies were performed in stable thyroparathyroidectomized dogs to evaluate the possibility of a direct renal action of vitamin D and its biologically active 25-hydroxylated metabolite. Alterations in renal hemodynamics and serum calcium concentration were minimized and attempts at vitamin D depletion were not undertaken. Steady-state volume expansion of modest degree was employed as the control experimental situation so that an effect of the vitamin to enhance phosphate reabsorption would not go undetected because of an already maximal phosphate reabsorptive rate secondary to parathyroidectomy. Under these experimental circumstances, 10,000 U of cholecalciferol and 25-120 U of 25-hydroxycholecalciferol (25-HCC) produced significant depressions in the percentage of filtered phosphate excreted (mean declines of 39 and 47%, respectively), which were not attributable to alterations in renal hemodynamics or to changes in the levels of serum calcium or phosphate. There was an accompanying decline in sodium and calcium excretion; mean percentage excretion rates for sodium fell by 38% with vitamin D and 26% with 25HCC, and for calcium this measurement declined by 46 and 23%, respectively. Furthermore, parathyroid hormone and 25HCC produced antagonistic effects on phosphate excretion. These observations provide the first conclusive evidence for a direct (proximal) tubular action of vitamin D to promote phosphate (as well as sodium and calcium) transport.

Animals↗

PubMed2000

The postmortem diagnosis of cholecalciferol toxicosis: a novel approach and differentiation from ethylene glycol toxicosis.

The objectives of this study were to develop a novel approach to postmortem diagnosis of cholecalciferol (CCF) toxicosis in dogs using kidney, bile, and urine samples, and to differentiate CCF from ethylene glycol (EG) toxicosis. To achieve these objectives, specimens collected from 2 previous laboratory studies in which dogs were given a single oral toxic dose of CCF (8.0 mg/kg) were used. For EG toxicosis, historical data from the previous 13 years (1985-1998) were reviewed and confirmed cases of EG toxicosis were selected. The historical data were used to compare trace mineral concentrations, specifically of calcium and phosphorus to differentiate between intoxications caused by CCF from that caused by EG in dogs. Kidneys, bile, and urine from dogs that died of CCF toxicosis were analyzed for 25 monohydroxy vitamin D3 (25(OH)D3) and 1,25 dihydroxy vitamin D3 (1,25(OH)2D3) and compared to known control unexposed dogs. Results of this study show that biliary and renal 25(OH)D3 concentrations and renal calcium to phosphorus ratio are of diagnostic value in dogs exposed to toxic concentrations of CCF. The renal calcium to phosphorus ratio was <0.1 in normal dogs, 0.4-0.9 in dogs that died of CCF toxicosis, and >2.5 in dogs that died of EG toxicosis.

Animals↗

PubMed1991

Effect of oral cholecalciferol supplementation at physiological and supraphysiological doses in naturally vitamin D3-deficient subterranean damara mole rats (Cryptomys damarensis).

The damara mole rat, Cryptomys damarensis, is a strictly subterranean dwelling herbivorous rodent that in its natural habitat has no access to any obvious source of cholecalciferol (D3). We examined the effects of D3 supplementation, at physiological and supraphysiological doses, on calcium metabolism, plasma concentrations of calcium and alkaline phosphatase (ALP) and D3 metabolites. Animals not receiving a D3 supplement maintained normal plasma calcium concentrations. In addition, they exhibited a high apparent fractional mineral absorption efficiency (91%) and maintained a positive mineral flux. The serum concentration of 25-(OH)D3 was undetectable (less than 5 nmol/l) and that of 1,25-(OH)2D3 was 41 +/- 10 pmol/l. Supplementation at a physiological dose of D3 resulted in increased plasma concentrations of D3 metabolites, food intake, apparent fractional absorption efficiency and apparent fractional retention efficiency. Despite the 1.8-fold increase in food intake, body mass remained constant suggesting that the enhanced energy intake was dissipated in catabolic processes. Plasma calcium and ALP concentrations were not significantly altered with physiological doses of D3. The group given supraphysiological doses of D3 exhibited hypercalcaemia, increased creatinine concentrations and markedly increased ALP levels. These data indicate that a pathological response to D3 intoxication occurred and that hepatic and renal excretory functions were impaired. It appears, therefore, that these animals function optimally at the low concentrations of D3 metabolites found naturally. Supplementation at both physiological and supraphysiological doses of D3 may disadvantage the damara mole rat.

Alkaline Phosphatase↗

PubMed1990

Effect of toxic doses of cholecalciferol (vitamin D3) on alkaline phosphatase levels in serum and gingival tissues of rats.

Toxic doses of cholecalciferol (vitamin D3) were injected subcutaneously (25 micrograms/day) into rats for 5 weeks, causing a significant increase of serum alkaline phosphatase (ALP) levels (p less than 0.01). Gingival tissue alkaline phosphatase levels were also elevated (p less than 0.01). On the other hand, a significant difference was detected between serum calcium levels in experimental and control groups (p less than 0.02).

Alkaline Phosphatase↗

PubMed1978

The effect of aflatoxin B1 on the utilization of cholecalciferol by chicks.

The official A.O.A.C. (1975) vitamin D3 chick assay of bone ash was used in a study of the effect of aflatoxin B1 (AFB1) on calcification and the utilization of cholecalciferol. U.S.P. vitamin D3 reference oil (D3) was mixed into the assay diet to give 0, 50, and 100 ICU D3/kg of diet. At each level of D3, AFB1 (Calbiochem) was mixed into the diet to give concentrations of 0, .5, 1.0, 5.0, 10.0, and 20 ppm. Individual bone ash values were determined at 3 weeks of age. These bone ash values were evaluated by a multiple regression analysis for two independent variables. A highly significant regression equation demonstrated a significant interaction between AFB1 and D3 on bone calcification. The equation indicates that 1 ppm of AFB1 in the ration increases the D3 requirement of the chick by 8.84 ICU/kg of diet.

Aflatoxins↗

PubMed1992

The effect of sodium zeolite A and cholecalciferol on plasma levels of 1,25-dihydroxycholecalciferol, calcium, and phosphorus in commercial Leghorns.

Three experiments were conducted to determine possible mechanisms involved in improving eggshell quality with sodium zeolite A (SZA) (trade name Ethacal feed component), and cholecalciferol (vitamin D3) by studying the effect of dietary supplementation of SZA and vitamin D3 on plasma 1,25-dihydroxycholecalciferol [1,25-(OH)2 D3], ionic calcium (Ca++), normalized calcium (nCa++), total calcium (TCa), percentage Ca++ to TCa (PCa++), pH, and phosphorus (P). In Experiment 1 (2 x 2 factorial arrangement of treatments), two levels of SZA (0 and .75%) and two levels of vitamin D3 (0 and 175 ICU/kg) were fed. In Experiment 2, five levels of vitamin D3 (100 to 500 ICU/kg) and two levels of SZA (0 and .75%) were fed using a 2 x 5 factorial arrangement of treatments. In Experiment 3, hens were fed two levels of SZA (0 and .75%). Blood samples were collected at 0 (Experiments 1, 2, and 3), 7, 14, and 21 h (Experiment 3) postoviposition (POP). In Experiments 1 and 2, decreasing vitamin D3 decreased plasma 1,25-(OH)2 D3 and P. Plasma TCa decreased when 0 ICU vitamin D3 was fed (Experiment 1), but was not affected by vitamin D3 level in Experiment 2. Supplemental SZA had no effect on plasma 1,25-(OH)2 D3, TCa, or P in Experiments 1 and 2. In Experiment 3, plasma 1,25-(OH)2 D3 and P peaked at 14 h POP, but Ca++ was lowest at 14 h POP. Circadian rhythms for plasma 1,25-(OH)2 D3, Ca++, and P were not affected by SZA. There were no significant effects due to dietary SZA on plasma 1,25-(OH)2 D3, TCa, Ca++, PCa++, nCa++, pH, or P.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum Silicates↗