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PubMed1995

25-hydroxycholecalciferol in poultry nutrition.

Vitamin D is a complex of secosteroids that must undergo metabolic alterations to reach optimal biological activity. The parent compounds 1) ergocalciferol (D2) and 2) cholecalciferol (D3) can be synthesized in the leaves of many plants or in the skin of most animals, respectively. Transport of vitamin D steroids after absorption is associated with vitamin D binding proteins (DBP). In general, the relative binding affinities of the vitamin D steroids are: 25-hydroxy vitamin D3 [25-(OH)D3] = 24,25-dihydroxy vitamin D3 [24,25-(OH)2D3] = 25,26-dihydroxy vitamin D3 [25,26-(OH)2D3] > 25-hydroxy vitamin D2 (25-(OH)D2) > 1,25-dihydroxy vitamin D3 [1,25-(OH)2D3] > vitamin D3. The DBP in poultry does not bind D2 forms effectively, and therefore poultry can not use this form of vitamin D adequately. The concentration of 25-(OH)D3 in blood seems to be well correlated with dietary vitamin D intake or exposure to ultraviolet light. The 1 alpha hydroxylase enzyme in the kidney is subject to negative feedback regulation and is critical for formation of the active metabolite 1,25-(OH)2D3. The intracellular vitamin D receptor (VDR) specifically binds 1,25-(OH)2D3 and is necessary for cellular action. Increased levels of two to three orders of magnitude are required for 25-(OH)D3 to compete with 1,25-(OH)2D3 for binding on VDR. Feeding studies with 25-(OH)D3 suggest it has nearly twice the activity of vitamin D3. Hatchability studies have shown that 25-(OH)D3 supports good fertility and hatchability, whereas hens fed only 1,25-(OH)2D3 did not have normal hatchability. Likewise, 1,25-(OH)2D3 seems to reach toxic levels at dietary concentrations only two to three times optimal dietary levels whereas feeding 25-(OH)D3 for extended periods at levels 8 to 10 times requirement seems to have no adverse effects. It seems that 25-(OH)D3 is the most active metabolite of vitamin D3, ultimately capable of supporting both cellular functions and embryonic development in chickens and turkeys when fed as the sole source of vitamin D3.

Animal Nutritional Physiological Phenomena↗
PubMed1996

N-acetyl-beta-D-glucosaminidase as a marker of renal damage in hens.

Urinary N-acetyl-beta-D-glucosaminidase (NAG) is an early physiological indicator of renal damage in several mammalian species. A study was conducted to confirm occurrence of NAG in hen urine, to establish baseline urinary NAG in laying hens, and to assess the feasibility of using the enzyme as a marker of renal damage in hens. Hy-Line hens were used in a completely randomized block design in the first part of the study. Urine was collected at 4 to 6, 6 to 10, 10 to 14, and 14 to 18 h, and serum at 4, 6, 10, and 14 h postoviposition, and assayed by spectrophotometry for NAG. Kidney tissue from additional hens was assayed histochemically for NAG. Serum NAG (range: 0.11 to 0.14 mU/mg protein) was found to be several orders of magnitude lower than urine NAG (6.44 to 12.27 mU/mg protein). Urine NAG increased from 4 to 6 h through 14 to 18 h, indicating that time of collection is critical in order to utilize the enzyme as a valid marker for laying hens. A preliminary study with five hens indicated that 10 d of treatment with liquid cholecalciferol (D3) supplement (three times the recommended level) were not enough to detect renal damage on the basis of significant changes in urine (NAG, but elevated urine NAG was detected at 40 d of D3-supplementation. Overall the results indicate that NAG in urine of laying hens is a potentially useful diagnostic marker of renal damage.

Acetylglucosaminidase↗
PubMed2001

Vitamin D deficiency in mothers of infants with rickets.

OBJECTIVE: To identify infants treated for vitamin D deficiency rickets, and to determine the incidence of vitamin D deficiency in their mothers and their mothers' country of origin. DESIGN: A retrospective audit of the medical records of children diagnosed with vitamin D deficiency rickets. Inpatients were identified by discharge diagnoses of vitamin D deficiency or hypocalcaemia and outpatients by pharmacy dispensing of cholecalciferol. SETTING: The Women's and Children's Health Care Network and the Southern Health Care Network (Melbourne, VIC) from June 1994 to February 1999. PATIENTS: 55 children with vitamin D deficiency rickets. RESULTS: Fifty-four of the 55 children were born to mothers with ethnocultural risk factors for vitamin D deficiency. Vitamin D status had been assessed in 31 of the 55 mothers (56%): 25 (81%) had 25-hydroxyvitamin D3 concentrations < or = 25 nmol/L, consistent with osteomalacia. CONCLUSION: Vitamin D deficiency continues to occur in children of migrant families. When infants are diagnosed with vitamin D deficiency, vitamin D levels in their mothers and siblings should also be assessed.

Adolescent↗
PubMed1999

Use of pamidronate to reverse vitamin D3-induced toxicosis in dogs.

OBJECTIVES: To determine whether pamidronate disodium can reduce vitamin D3-induced hypercalcemia in dogs and whether combination treatment with calcitonin is more effective than treatment with pamidronate alone. ANIMALS: 20 clinically normal male Beagles. PROCEDURE: All dogs were given 8 mg of cholecalciferol (CCF)/kg of body weight once orally, then were assigned randomly to 4 groups of 5 dogs each. Dogs were given 0.9% NaCl solution IV (group 1), calcitonin SC and 0.9% NaCl solution IV (group 2), pamidronate and 0.9% NaCl solution IV (group 3), or a combination of all 3 agents (group 4). Dogs were observed for 28 days, and serial blood and urine samples were collected for determination of serum biochemical, electrolyte, and 25(OH)D3 values, CBC, and urine mineral excretion. Samples of kidney, stomach, lung, aorta, liver, duodenum, and brain were evaluated by light microscopy and quantitative mineral analysis. RESULTS: Two dogs in group 1 were euthanatized 4 days after CCF administration because of severe clinical signs of disease. Dogs in group 3 lost less weight and had significantly lower serum phosphorus, total and ionized calcium, and urinary zinc concentrations, compared with dogs in group 1. On day 4, serum urea nitrogen concentration was significantly lower in dogs of groups 3 and 4, compared with dogs in group 1. Mild to moderate mineralization of kidneys and stomach were observed in the 2 group-1 dogs euthanatized on day 4. CONCLUSIONS: Pamidronate administration effectively prevents CCF-induced hypercalcemia and mineralization of soft tissues. CLINICAL RELEVANCE: Pamidronate is a potentially useful antidote against CCF toxicosis in dogs.

Analgesics↗
PubMed2000

Comparison of commercially available (125)I-based RIA methods for the determination of circulating 25-hydroxyvitamin D.

BACKGROUND: Measurement of circulating 25-hydroxyvitamin D [25(OH)D] is important in the management of metabolic bone disease. The aim of this study was to compare two widely used methods for the quantification of circulating 25(OH)D with attention to their abilities to measure 25-hydroxylated ergocalciferol (vitamin D(2)) [25(OH)D(2)] and cholecalciferol (vitamin D(3)) [25(OH)D(3)]. METHODS: We used two commercially available, Food and Drug Administration-approved, radioiodine ((125)I)-based RIA kits for the detection of 25(OH)D (DiaSorin, Stillwater, MN and IDS Ltd, Tyne and Wear, United Kingdom). These methods were tested for general assay performance, including antibody specificity. Results were compared with those of an HPLC-based direct ultraviolet detection method. RESULTS: Within- and between-run CVs were </=10%. Both methods quantitatively recovered 25(OH)D(3) added to serum, but only the DiaSorin kit quantitatively recovered 25(OH)D(2). The primary antibody in the IDS kit had unequal reactivities with pure 25(OH)D(2) and 25(OH)D(3), whereas the DiaSorin primary antibody reacted with them equally. In 50 patient samples assayed by HPLC, the IDS method, but not the DiaSorin method, underestimated total circulating 25(OH)D when significant circulating 25(OH)D(2) was present in patient samples. CONCLUSIONS: Some immunoassays may underestimate total 25(OH)D when 25(OH)D(2) constitutes an appreciable part of the total.

Adolescent↗
PubMed2003

The effect of vitamin D3 on insulin secretion and peripheral insulin sensitivity in type 2 diabetic patients.

The aim of this study was to evaluate the effect of vitamin D3 supplementation on insulin secretion and insulin resistance. Ten females with type 2 diabetes being treated with oral hypoglycaemic agents and with normal serum and urine calcium levels were enrolled in the study. The study was conducted in March, when levels of vitamin D are lowest in our region. The level of plasma 25(OH)D was measured (normal range in winter 25-120 nmol/l). The first (FPIS) and second (SPIS) phases of insulin secretion were studied during IVGTT. Peripheral insulin resistance was measured. A group of 17 age- and BMI-matched females with normal glucose tolerance served as a control group. The diabetic patients were treated with cholecalciferol 1332 IU daily for one month. The mean plasma 25(OH)D level was 35.3 +/- 15.1 nmol/l at baseline, 70% of patients being vitamin D deficient. After one month of treatment with vitamin D3, the plasma 25(OH)D level increased by a mean of 75.8%; 70% of the patients achieved normal vitamin D levels. FPIS increased significantly by 34.3%, while the change in SPIS of 20.4% was not significant (p > 0.8). We found a significant correlation between the change in FPIS and the change in 25(OH)D level after vitamin D3 supplementation (p < 0.018). The results showed a decrease of 21.4% in insulin resistance after one month, but the change was not significant. Bearing in mind that the main defects in type 2 diabetes mellitus are reduced FPIS and insulin resistance, and the favourable effect vitamin D3 had on them, we suggest vitamin D3 deficiency may at least partly contribute to the impairment of insulin secretion and probably of insulin action. Our results suggest that vitamin D3 supplementation could be an element in the complex treatment of type 2 diabetes mellitus during the winter.

Adult↗
PubMed2003

[Vitamin D3 overdosage due to rashly diagnosed rachitis in a child with distal tubular acidosis].

Metabolic acidoses are diseases causing many diagnostic and therapeutic problems. Compensated metabolic acidosis can be unrecognised for a long time. This refers especially to isolated renal tubular acidosis (RTA). Unrecognised RTA causes calcium and phosphorus balance disturbances with clinical signs of improper bone mineralization. It happens that some patients with mentioned problems are "treated" as rachitic and take high doses of vitamin D. As a result, serum calcium and phosphates as well as urine calcium increase, without the satisfied influence on bone mineralization. We present a case of a 3.5 months old baby, who was "treated" as ricket in vitamin D deficiency. This baby was "cured" with high doses of cholecalciferol (0.0875 mg/24h for 2 weeks, then 0.175 mg/24h for 3 weeks) because of craniotabes. This treatment was carried on without any metabolic tests and caused the following disturbances: 25(OH)D serum level - 102.7 ng/ml (normal 11-54), 1,25(OH)2D serum level - 39.5 pg/ml (normal 15-70), calcaemia 2.7-2.85 mmol/l, phosphataemia 2.1 mmol/l. In this time the considerable hipercalciuria (second morning urine sample Ca/cr ratio 2.06 mmol/mmol) occurred. The other laboratory test showed as follows: serum albumins 4.5 g/dl, alkaline phosphatase 188 U/l, acid phosphatase 10.7 U l, Cl- 114.9 mmol/l, Na 146 mmol/l, K 4.8 mmol/l, HCO3a 16.6-20.1 mmol/l and pCO2 3.63-3.85 kPa, serum anion gap 11 mEq/l; pH of morning urine 6.5-7. These results suggested the presence of distal RTA aside from symptoms of vitamin D overdosage. The high serum levels of calcium and phosphates, craniotabes, rather low serum alkaline phosphatase activity and presence of metabolic acidosis the symptoms after the normalisation of calcium and phosphorus balance suggested that the distal RTA had been prior to calcium disturbances.

Acidosis, Renal Tubular↗
PubMed2005

Vitamin D deficiency among patients attending a central New Zealand rheumatology outpatient clinic.

AIMS: To measure the Vitamin D status in patients attending a rheumatology outpatient clinic because of the known musculoskeletal and immunosuppressive effects of Vitamin D deficiency. METHODS: 66 consecutive patients at a private rheumatology clinic in central New Zealand were recruited at the beginning of winter. RESULTS: Of 66 patients, 55 patients were included in the analysis. 43 (78%) had 25OH cholecalciferol levels that were below the reference range (50-150 nmol/L), and of these 12 (22%) had levels classified as moderate to severe deficiency (<25 nmol/L). CONCLUSIONS: Vitamin D deficiency is common in this setting, and is likely to contribute to the musculoskeletal symptoms experienced in this population.

Adolescent↗
PubMed2005

Which therapy to prevent post-thyroidectomy hypocalcemia?

Hypocalcemia is one of the most frequent complications after total extracapsular thyroidectomy (TET). In most of cases it is a transient phenomenon. The aim of this study is to evaluate if and how the oral administration of calcium or calcium combined with D-vitamin could effectively prevent post-thyroidectomy hypocalcemia. A randomized prospective study was performed, recruiting 120 patients who underwent total thyroidectomy. The patients in our series were randomly assigned to one of two groups: group A--patients who received calcium lactogluconate/calcium carbonate (mg 300 per day); group B--patients who received calcium carbonate/cholecalciferol therapy (calcium carbonate: 1500 mg per day; cholecalciferol 400 UI per day). The groups were well matched for age, sex and pathologies. Patients of both A and B groups were divided in two subgroups: those operated on for benign thyroid diseases (A1 and B1) and those operated on for malignancy (A2, B2). Serum calcium assays, performed 24, 48 and 72 hours after surgery, showed mean values of calcemia higher in patients of the B1 and B2 group. Statistical analysis was performed using a Student's t test. Mean serum calcium concentrations on post-operative day one, two and three were higher in patients of the group B (p<<0.01). Early and combined oral administration of both calcium and vitamin D seemed to prove major efficacy in preventing and treating post-operative hypocalcemia, showing mean serum calcium levels higher than those of patients who received only oral calcium administration. Nevertheless, further studies are necessary to validate these data.

Adult↗
PubMedDate not supplied

[Metabolism of vitamin D3 administered in liposomes in rat liver].

Incorporation of [3H]-cholecalciferol into the liver and the rate of its conversion into 25-OH-D are significantly larger after intravenous administration of this vitamin into liposomes than its dissolution in ethanol. The latter may be due to a different distribution of vitamin D3 in the cells of the liver. Incorporation of [3H]-vitamin D3 in reticulocytes suggests that its cells are a locus for storage of vitamin D, from which the latter is transported into hepatocytes where its 25-hydroxylation proceeds.

Animals↗
PubMed1975

Studies of vitamin D deficiency in man.

Highly sensitive assays have been developed that enable 25-hydroxycholecalciferol (25-hydroxyvitamin D3) and 25-hydroxyergocalciferol (25-hydroxyvitamin D2) to be measured in the same serum sample. With these assays it has been shown that endogenously produced cholecalciferol (vitamin D3) is important in man; the findings further emphasize the role of vitamin D metabolites as hormones rather than vitamins in the traditional sense. Dietary sources of vitamin D appear to be inadequate and vitamin D deficiency has been shown to the cause of rickets and osteomalacia in Asian immigrants to Britain. This condition may be readily treated with small doses of vitamin D. In addition, sub-clinical deficiency was found in the Asian community. In the elderly, also, vitamin D deficiency was established as an important cause of osteomalacia and again evidence for the existence of a sub-clinical deficiency state was found. It is therefore suggested that the present prophylactic practices should be reviewed. Secondary hyperparathyroidism (reflected by elevated concentrations of circulating immunoassayable parathyroid hormone) was shown to be the rule rather than the exception in vitamin D deficiency. Some patients, however, had failed to respond to a hypocalcaemic stimulus. In others, there were high concentrations of parathyroid hormone despite normal serum calcium concentrations. Thus the relationship between parathyroid hormone and metabolites of vitamin D may not be mediated through changes in serum calcium alone, and it is postulated that metabolites of vitamin D may directly affect the secretion of parathyroid hormone.

Adolescent↗
PubMed1977

[Enzootic calcinosis and other plant induced calcinoses (author's transl)].

A review is given of the literature concerning the so-called plant induced calcinosis in animals (tabel I), i.e. diseases which in their patological-anatomical appearance show great similarities with vit. D-intoxication. The etiology of the diseases are discussed in view of the last 5--10 years rapid development of knowledge concerning vit. D3 metabolism. It is pointed out that the most recent results indicate that enzootic calcinosis is caused by a 1,25-dihydrocholecalciferol-glycoside, which is hydrolysed in the intestinal tract. By this reaction 1.25 (OH) 2 cholecalciferol--the biological active metabolite of vit. D3 -- is set free, and thus able to act directly on the intestinal absorption mechanism. By this reaction the point of calcium metabolism regulation is essentially by-passed and calcium and phosphate absorption proceeds essentially out of control, causing hypercalcaemia, hyperphosphataemia, hypersecretion of calcitonin and calcinosis.

Animals↗
PubMed1977

[Vitamin A-vitamin D3 relationship in growing rats].

A relation vitamin A - vitamin D3 exists in diet for growing rats. When this decreases from 5 (microgram A - IU D3) or 15 (IU A - IU D3) to 1,25 (microgram/IU) or 3,75 (IU/IU) growth, calcemia are increasing but vitamin A hepatic storage is decreasing. In other words for a same quantity of retinol, cholecalciferol's level in diet determines hepatic stores of vitamin A. General aspect of this question is discussed.

Animal Nutritional Physiological Phenomena↗
PubMed1977

High pressure liquid chromatographic separation and identification of vitamins D2 and D3 in the presence of fat-soluble vitamins in dosage forms.

A simple and rapid qualitative method is described for determining the presence of vitamin D2 (ergocalciferol) and/or vitamin D3 (cholecalciferol) in various preparations by reverse phase high pressure liquid chromatography (HPLC). When both D2 and D3 are present, this method effectively separates and identifies each vitamin D form by its respective retention time. A significant difference between vitamins D2 and D3 exists in their antirachitic activity in poultry. Preparations can be tested rapidly by this method to ascertain that the correct D vitamin form has been added. Fat-soluble vitamins such as vitamins A, E, K1, and K3 do not interfere. Vitamins D2 and D3 were separated at the baseline in model preparations. As little as 2 ng each of vitamin D2 and vitamin D3 can be separated and identified.

Cholecalciferol↗
PubMed1978

Analysis of fat-soluble vitamins. XX. Determination of vitamin D in multivitamin preparations. Second collaborative study.

The official first action method for determining vitamin D in multivitamin preparations was modified. The method was collaboratively studied by 7 laboratories, using 6 preparations in oil. The preparations consisted of vitamin D at various levels and at various ratios (in w/w) in vitamin A. Three samples contained cholecalciferol and 3 samples contained vitamin D3 from vitamin D3 resin. After outliers were eliminated by the Dixon test, data were analyzed and averages were compared with amounts of vitamin D known to be in each sample. For samples with vitamin D: vitamin A ratios of 1:0.5, 1:5, and 1:10, the mean vitamin D recoveries were 98.8, 94.6, and 90.7%, respectively. The method has been adopted as official final action.

Cholecalciferol↗
PubMed1990

Salmon calcitonin as adjunct treatment for vitamin D toxicosis in a dog.

Calcitonin was used in conjunction with saline diuresis, furosemide, and prednisone in treatment of a dog that consumed a rodenticide that contained cholecalciferol and has been touted as safe for nontarget species. This report shows that the rodenticide is toxic to dogs and that salmon calcitonin is a useful treatment for the often refractory hypercalcemia induced by vitamin D toxicosis.

Animals↗
PubMed1979

Naturally occurring vitamin D3 in fish products analysed by HPLC, using vitamin D2 as an international standard.

A chemical method for the analysis of naturally occurring vitamin D is proposed. The unsaponifiable matter of oils and tissues is prepared, cholesterol is partly removed by double precipitation at low temperature in methanol. The vitamin D fraction is collected on an adsorption column by high performance liquid chromatography. The fraction is further purified and the vitamins D2 and D3 are separated on a partition column (reverse phase) by HPLC. Recovery was 89 to 93%, standard deviation 3%. The only vitamin D analogue found in fish oils, livers and fillets, was cholecalciferol (D3). Hence, ergocalciferol (D2) could be used as an internal standard. The provitamins ergosterol and 7-dehydrocholesterol, as well as the previtamins, were separated from the vitamin D-fraction on the adsorption column. Results in the range 0.050 to 134 microgram D3 per gram (2 to 5360 I.U. per gram) are given. One cod liver oil was analysed in a rat bioassay, giving supporting results.

Adsorption↗
PubMedDate not supplied

[Comparative study of the hemolytic action of group D vitamins].

Hemolytic effects of the vitamins of the D group (ergocalciferol - D2, cholecalciferol - D3, and 1 alpha-hydroxycholecalciferol - 1 alpha-OH-D3) were compared using rat erythrocytes. The latent period of hemolysis, caused by 1 alpha-OH-D3 was approximately 3-fold shorter as compared with the hemolysis caused by D2 or D3. Apparent values for energy of activation of hemolysis, estimated at 30-45 degrees, constituted for D2 - 23.2 kcal/mol, D3 - 25.3 kcal/mol, 1 alpha-OH-D3 - 13.1 kcal/mol. Despite the higher hemolytic activity, the rate of 1 alpha-ON-D3 autooxidation was distinctly lower than that of D3.

Animals↗