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Query: UMLS:C0205700 (ash)
 15,125 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The research described in this paper relates the changes in serum concentration of calcium, phosphorus, and 1,25-dihydroxycholecalciferol [1,25(OH)2D3] to changes in tibial ash percentage and the incidence of endochondral ossification defects (EOD) in flocks of commercially reared broiler chickens at 14 d of age. Sequential studies of six Australian broiler flocks representing three major genetic lines were undertaken at weekly intervals from 1 to 28 d of age. Serum collected from birds was analyzed for total calcium, inorganic phosphorus, and 1,25(OH)2D3. Tibial ash percentage was also determined at weekly intervals, and the incidence of EOD was determined at 14 d of age by examining sagittal sections of the proximal tibiotarsus. The EOD observed in the 14-d-old broiler chickens were characterized by enlarged zones of proliferating chondrocytes, similar to that which occurs during calcium- or vitamin D-dependent rickets. Three flocks had a 50% incidence of EOD at 14 d of age and were classified as severely affected. The other three flocks had incidences ranging from 12 to 16% and were classified as mildly affected. Broiler flocks severely affected with EOD (50% incidence at Day 14) had lower (P < or = .05) concentrations of 1,25(OH)2D3 than flocks mildly affected (12 to 16% incidence). Tibial ash percentages were lower (P < or = .05) in the severely affected flocks between Days 14 to 28, and it is likely that a lower rate of ash accretion between Days 7 to 14 precedes the development of the EOD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Serum total calcium, phosphorus, 1,25-dihydroxycholecalciferol, and endochondral ossification defects in commercial broiler chickens. 797 74

The mechanism of aluminum (Al) toxicity may involve disturbances in calcium (Ca) metabolism. Aluminum compounds have been reported to reduce vitamin D-dependent Ca absorption in chicks, rats and humans. To investigate the mechanism by which Al reduces Ca absorption, we studied the effect of dietary aluminum chloride (AlCl3) on the relative amounts of intestinal calbindin D-28K in chicks fed diets varying in Ca and phosphorus concentration. AlCl3 was added so that Al constituted 0, 0.15 or 0.3 g/100 g of diets that were either adequate, low in Ca, low in P, or contained supplemental P. Diets were fed for 2 wk. Intestinal calbindin D-28K levels were assayed using SDS-PAGE and 45Ca binding to Western blots. Added dietary Al greatly reduced the amount of intestinal calbindin in chicks fed adequate diets, low Ca diets, or low P diets. When diets with supplemental P were fed, little calbindin was evident with or without added Al. Tibia ash, body weight and food intake were also reduced (P < 0.05) by added Al. These results indicate that dietary AlCl3 inhibits vitamin D-dependent Ca absorption by reducing the amount of intestinal calbindin D-28K. Aluminum, therefore, may interfere with the body's ability to regulate intestinal calbindin D-28K levels. This could have implications for other tissues that contain substantial levels of calbindin D-28K.
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PMID:Dietary aluminum chloride reduces the amount of intestinal calbindin D-28K in chicks fed low calcium or low phosphorus diets. 822 92

Three experiments were conducted to examine the efficacy of dietary 1,25-dihydroxycholecalciferol [(1,25-(OH)2D3)] on the development of tibial dyschondroplasia (TD) in chickens divergently selected for high (HTD) and low (LTD) incidences of TD. In Experiment 1, chickens from the two lines were fed two calcium levels (0.75 and 1.0%), with and without 5 micrograms/ kg dietary 1,25-(OH)2D3. In Experiment 2, both lines were fed diets containing 1.0% calcium and 0, 5, 10, or 15 micrograms/kg 1,25-(OH)2D3. The addition of 1,25-(OH)2D3 did not reduce the overall incidence of TD in Experiment 1, but did reduce the incidence of severe TD from 69 to 48% in the chickens receiving the 0.75% calcium diet. In this experiment, LTD chickens had higher plasma phosphorus and bone ash. No line differences were noted between plasma vitamin D metabolites or intestinal vitamin D receptors. In Experiment 2, 5 micrograms/kg of 1,25-(OH)2D3 decreased the incidence of TD from 94 to 76% and number three scores from 69 to 44% (P < or = 0.001). Higher amounts of 1,25-(OH)2D3 further decreased TD, but there was a reduction in body weight above 5 micrograms/kg. Plasma 25-hydroxycholecalciferol [25-(OH)D3] and 1,25-(OH)2D3 were higher and intestinal vitamin D receptors were lower in HTD chickens than in LTD chickens. Plasma 1,25-(OH)2D3 was not affected by dietary treatment, but 25-(OH)D3 was reduced by dietary 1,25-(OH)2D3. Experiment 3 was conducted to examine effects of line and dietary 1,25-(OH)2D3 on plasma vitamin D metabolites and intestinal and growth plate receptors. No effect of genetic line or dietary 1,25-(OH)2D3 was observed for vitamin D receptors concentration or plasma 1,25-(OH)2D3 levels. Plasma 25-(OH)D3 was reduced when 1,25-(OH)2D3 was fed. These results indicate that HTD chickens are somewhat responsive to dietary 1,25-(OH)2D3, but this treatment failed to prevent the lesion in a large portion of the population.
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PMID:Dietary 1,25-dihydroxycholecalciferol has variable effects on the incidences of leg abnormalities, plasma vitamin D metabolites, and vitamin D receptors in chickens divergently selected for tibial dyschondroplasia. 905 17

Four experiments were conducted to investigate the effects of ultraviolet (UV) light exposure and several cholecalciferol metabolites on the development of tibial dyschondroplasia (TD) and other parameters associated with vitamin D metabolism in chickens selected for high (HTD) and low (LTD) incidence of TD. In Experiment 1, exposure of chickens to UV light reduced the incidence and severity of TD more in LTD chickens than in HTD chickens, as evident by the significant interactions (P < 0.10 and 0.04). In Experiment 2, the addition of cholecalciferol to diets that were deficient in cholecalciferol linearly decreased the incidence of vitamin D rickets and increased bone ash, but increased the incidence of severe TD. The LTD chickens had a higher maximal bone ash of 40.0 +/- 0.7% than did the HTD chickens, which had a maximal bone ash of 37.0 +/- 0.7%. In Experiment 3, the addition of 5 micrograms/kg of 25-hydroxycholecalciferol [25-(OH)D3], 1-alpha-hydroxycholecalciferol, or 1,25- dihydroxycholecalciferol decreased the incidence and severity of TD in the LTD chickens and had no effect on TD in HTD chickens. In Experiment 4, increasing dietary 25-(OH)D3 increased plasma 25-(OH)D3 levels in both lines, but HTD chickens had higher plasma 25-(OH)D3 levels at 20 and 40 micrograms/kg of dietary 25-(OH)D3. The incidence and severity of TD were reduced in the LTD chickens by dietary 25-(OH)D3, but little effect was noted in HTD chickens. The LTD chickens reached a maximal bone ash at 9.7 +/- 1.9 micrograms/kg and HTD chickens reached the same bone ash at 33.0 +/- 7.0 micrograms/kg. These results indicate that UV light and vitamin D metabolites are not effective in preventing TD in HTD chickens, but that altered vitamin D metabolism does exist between HTD and LTD chickens.
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PMID:The effects of ultraviolet light and cholecalciferol and its metabolites on the development of leg abnormalities in chickens genetically selected for a high and low incidence of tibial dyschondroplasia. 905 18

Sex steroids were suggested as regulators of vitamin D metabolism. While considerable data is available regarding interaction between estradiol and vitamin D, very little is known about interactions between testosterone and vitamin D. A similar gap exists with regard to the involvement of the vitamin D endocrine system in the pathogenesis of the female versus the male osteoporosis syndrome. In the present study we studied the effect of long-term treatment with testosterone on the metabolism of vitamin D in vitamin D3 replete sexually immature male chicks. We were able to show under this treatment, circulating levels of 1,25-dihydroxy vitamin D3 (1,25(OH)2D3) are significantly reduced, but intestine and bone concentrations are significantly increased. The increased concentration of 1,25(OH)2D3 in bone was accompanied by an increase in the ash content of this tissue. The reduction in serum 1,25(OH)2D3 was not dependent on reduced activity of the renal 25-hydroxy vitamin D3 - alpha - hydroxylase. Based on these findings it is proposed that testosterone is involved in the stimulation of the biological response to vitamin D in the classical target-organs, such as intestine and bone, and this observation may provide partial explanation to the pathogenesis of osteoporosis in hypogonadal men.
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PMID:The metabolism of vitamin D3 in response to testosterone. 911 69

In 1996, the National Institute of Standards and Technology (NIST) released Standard Reference Material 1846 (Infant Formula), which can be used as a control material for assigning values to in-house control materials and for validating analytical methods for measurement of proximates, vitamins, and minerals in infant formula and similar matrixes. The SRM was manufactured by preparing a spray-dried formula base containing fat, protein, carbohydrates, and minerals and then combining that formula base with a dry-blend vitamin premix that supplied the vitamins. The Certificate of Analysis for SRM 1846 provides assigned values for concentrations of proximates (fat, protein, etc.), vitamins, and minerals for which product labeling is required by the Infant Formula Act of 1980 and by the Nutrition Labeling and Education Act of 1990. These assigned values were based on agreement of measurements by NIST and/or collaborating laboratories. Certified values are provided for vitamins A (trans), E, C, B2, and B6 and niacin. Noncertified values are provided for solids, ash, fat, nitrogen, protein, carbohydrate, calories, vitamin D, delta-tocopherol, gamma-tocopherol, vitamin B1, vitamin B12, folic acid, pantothenic acid, biotin, choline, inositol, calcium, phosphorus, magnesium, iron, zinc, copper, sodium, potassium, and chloride. Information values are provided for iodine, manganese, selenium, and vitamin K.
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PMID:Certification of nutrients in Standard Reference Material 1846: infant formula. 917 Jun 57

Groups of weanling pigs (5 castrated males, 5 females per group) were fed purified diets containing the NRC's requirements for nutrients and 0, 1.1, 4.4 or 7.7% olestra for 12 wk. Graded concentrations of vitamins A, D2 and E were added at each olestra concentration. The primary purpose of the study was to establish relationships between dietary concentration of olestra and the amounts of vitamins A, D2 and E needed to restore tissue concentrations of these vitamins to control concentrations. A secondary purpose was to confirm that olestra does not affect the status of vitamin K or water-soluble nutrients. Liver concentrations of vitamins A, E and B12, iron and zinc and bone concentrations of ash, zinc, calcium and phosphorus, were measured in a group of pigs killed at the start of the study and in all pigs killed at wk 12. Growth, feed efficiency, hematology, clinical chemistry, blood concentrations of retinol, alpha-tocopherol, 25-hydroxyergocalciferol, 25-hydroxycholecalciferol, 1,25-dihydroxyvitamin D, folate, iron, total iron-binding capacity, zinc and calcium and adipose concentration of vitamin E were measured at 4-wk intervals. Prothrombin time was measured weekly for the control and 7.7% olestra groups, monthly for others. Relationships derived from measured tissue concentrations of vitamins A and E showed that constant amounts of the vitamins were required per unit mass of olestra in the diet to restore tissue concentrations to control values. Such a relationship could not be determined for vitamin D because exposure of the pigs to UV light resulted in an apparent interaction between vitamin D2 and vitamin D3. Olestra did not affect growth, digestible feed efficiency, vitamin K status or the status of the water-soluble micronutrients, in agreement with other studies in the pig.
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PMID:Olestra's effect on the status of vitamins A, D and E in the pig can be offset by increasing dietary levels of these vitamins. 923 57

The standard method for determination of density (g/cm3) of bones from small animals has been the application of Archimedes' principle. A recent development has been software for the determination of "density" (g/cm2) of small animal bones with dual-energy X-ray absorptiometry (DXA). We compared Archimedes' principle and DXA (Hologic QDR-2000) in the measurement of the densities of whole and hollowed femurs of 5- to 6-month-old retired female breeder rats. In an attempt to ensure detectable treatment differences, rats were used from a low-vitamin D Holtzman and a supplemental-vitamin D Sprague-Dawley colony. Whole femur densities were higher for supplemental-vitamin D colony rats than for low vitamin D rats using both techniques (Archimedes' principle, p < 0.002; DXA, p < 0.005), and the densities from the two techniques were highly correlated (r = 0.82, p < 0.0001). Actual density values were higher for Archimedes' principle than for DXA. Other variables such as femur ash weight and calcium content were also highly correlated to densities with both techniques. Hollowed femur density values were higher than whole femur values with Archimedes' principle but lower with DXA. Colony effects for hollowed femur densities were diminished with Archimedes' principle (p < 0.03) and eliminated with DXA (p < 0.53). Investigation of whole bones is more biologically relevant, and both techniques were effective in detecting differences between whole femurs from low-vitamin D and supplemental-vitamin D colony rats.
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PMID:Comparison of bone density measurement techniques: DXA and Archimedes' principle. 938 95

Three experiments were conducted to test the hypothesis that a vitamin D deficiency alters the immune responses of female broiler chicks. The control diet contained 800 IU of cholecalciferol (vitamin D3)/kg and the deficient diet was the same except without supplemental vitamin D3. The vitamin D deficiency status was established on the basis of a significantly lower blood ionized calcium or total serum calcium (75 to 85% of the control). Vitamin D-deficient chicks also had lower growth rate and bone ash. In Experiment 1 at 8 d of age, and Experiment 2 at 23 d of age, the cutaneous basophil hypersensitivity response as determined by the increase in interdigital skin thickness 20 h after a single injection of 100 microg phytohemagglutinin-P was significantly depressed in vitamin D-deficient chicks (62 to 64% of the control). Thymus weight, adjusted for body weight, was significantly lower in the vitamin D-deficient chicks at 24 d of age (61% of the control). Primary and secondary antibody responses against SRBC in vitamin D-deficient chicks were not different from the control. In Experiment 3, in 17-d-old chicks, vitamin D deficiency decreased the number of abdominal macrophages phagocytizing SRBC in vitro within 45 min from 14.7 to 10.1%. These results indicate that vitamin D deficiency depresses the cellular immune responses in young broiler chicks.
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PMID:Vitamin D deficiency alters the immune responses of broiler chicks. 962 32

This investigation was directed towards finding the need of vitamin D for fish. The freshwater column feeder fish Labeo rohita (Rora) was used for the study. Early fry stage fish were divided into four experimental groups of 350 each: two groups were kept in natural light, while the other two were maintained under total darkness. One each of the light and dark-grown groups was supplied dietary vitamin D3 [1,650 i.u/kg diet], whereas the other groups were fed a vitamin D-deficient diet for six months. The known vitamin D-related functions and growth parameters were studied in these four experimental groups of fish. The results showed that fish reared on vitamin D-deficient diet and in dark did not have even traces of liver vitamin D, indicating a state of vitamin D deficiency in these fish. No significant differences were observed in percent bone to body weight or dry matter of the vitamin D-deficient/supplemented groups of fish grown in light/dark. Further, it was also observed that there were no significant changes in bone and carcass ash or calcium and phosphorus content in response to vitamin D3 supplementation as compared to the groups which did not receive vitamin D3 (grown both in light and dark). Also, there was little change in several other parameters like carcass protein and lipid, mortality rates, hepatosomatic index, and feed efficiency between the vitamin D-deficient/supplemented groups of fish. Thus, these findings suggest that vitamin D may not be an essential nutrient for Rora (Labeo rohita) as a representative of freshwater fish.
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PMID:Vitamin D is not an essential nutrient for Rora (Labeo rohita) as a representative of freshwater fish. 967


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