Biomedical subjects

H M Edwards

Publications and source records attributed to H M Edwards.

At least 55 records · Page 3Linked to original sources

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

The effects of 1,25-dihydroxycholecalciferol and phytase on the natural phytate phosphorus utilization by laying hens.

Two experiments were conducted to investigate the effects of supplementing a corn-soybean layer diet with either phytase, 1,25-dihydroxycholecalciferol [1,25-(OH)2D3], or their combination. The basal diet was formulated to contain 3.00% Ca and 0.33% total P. In Experiment 1, 160, 56-wk-old laying hens were randomly assigned to treatment groups fed either the basal diet alone or diets supplemented with either 600 phytase units (FTU) per kilogram feed, 5 microg 1,25-(OH)2D3/kg feed, or their combination for an experimental period of 9 wk. Experiment 2 had the same design and treatment groups except that laying hens 24 wk of age were used for 8 wk. In both experiments, phytase had a positive effect on BW and increased plasma dialyzable P, tibia bone ash, and phytate P retention. In the first experiment, the addition of phytase, 1,25-(OH)2D3, or their combination prevented a rapid decrease in egg production due to a Mycoplasma gallisepticum infection observed in hens fed the basal diet. However, no benefit in egg production was obtained in the second experiment. No effects on egg weight and egg specific gravity were observed in both experiments. These results clearly indicate that phytase, and to a lesser extent 1,25-(OH)2D3, can be used to increase the utilization of phytate P by laying hens.

6-Phytase↗

PubMed1998

Bioavailability of iron in cottonseed meal, ferric sulfate, and two ferrous sulfate by-products of the galvanizing industry.

Iron depletion-repletion assays were carried out with young chicks to establish Fe bioavailability values for Fe2(SO4)3.7H2O (22.7% Fe), Fe-ZnSO4.H2O (20.2% Fe, 13.0% Zn), Zn-FeSO4.H2O (20.2% Zn, 14.2% Fe), and cottonseed meal (200 mg Fe/kg). Standard hemoglobin response curves were established using feed-grade FeSO4.H2O (28.8% Fe) or reagent-grade FeSO4.7H2O (20.1% Fe) as standards such that relative bioavailability (RBV) could be assessed for the experimental sources of Fe. Weight gain, hemoglobin, and hematocrit responded linearly (P < 0.05) to Fe supplementation in all assays. Using hemoglobin as the response criterion, slope-ratio calculations established Fe RBV values of 126% for Fe-ZnSO4.H2O and 93% for Zn-FeSO4.H2O. The 126% value for Fe-ZnSO4.H2O was greater (P < 0.05) than the FeSO4.H2O standard (100%), but the 93% value for Zn-FeSO4.H2O was not different (P > 0.10) from the standard. However, evaluation of all criteria of response (hemoglobin, hematocrit, weight gain) suggested that neither Fe-ZnSO4.H2O nor Zn-FeSO4.H2O had different Fe RBV values than FeSO4.H2O. Standard-curve calculations were used for assessment of Fe RBV in Fe2(SO4)3.7H2O and cottonseed meal, as only a single level of Fe addition was studied for each of these products. Iron RBV in Fe2(SO4)3.7H2O was estimated to be 37%, whereas Fe RBV in cottonseed meal was found to be 56%. Both of these values were lower (P < 0.05) than the FeSO4 standard. The data suggest that the two new products, representing combinations of FeSO4.H2O and ZnSO4.H2O by-products of the galvanizing industry, are excellent sources of bioavailable Fe, whereas ferric sulfate and cottonseed meal are relatively poor sources of usable Fe.

Animal Feed↗

PubMed1997

Maintenance threonine requirement and efficiency of its use for accretion of whole-body threonine and protein in young chicks.

Broiler chicks were fed on chemically-defined crystalline amino acid diets containing graded levels of L-threonine (Thr) during the period 10-20 d post-hatching. Doses of Thr represented 5, 10, 15, 40, 55, 70 and 95% of its ideal level for maximal weight gain and feed efficiency. Other amino acids were maintained at minimized excess levels that were 15% (of ideal) above the various doses of Thr. Following 10 d of feeding and a 24 h fast, chicks were killed for whole-body protein and amino acid analysis. Using pen accretion means, weight gain (r2 0.98), protein accretion (r2 0.99), and Thr accretion (r2 0.99) were linear (P < 0.01) functions of Thr intake. Slope of the Thr accretion regression line indicated that 82% of the Thr intake was recovered in whole-body protein. At zero Thr intake, chicks lost 11.9 mg Thr/d. The Thr maintenance requirement was 45.7 mg/d per kg body weight 0.75. Increasing doses of Thr resulted in increased (P < 0.05) concentrations of methionine, isoleucine, histidine and lysine in whole-body protein. Other indispensable amino acids, including Thr, also tended to increase. Whole-body glycine, proline, serine and cystine concentrations decreased (P < 0.05) as Thr was increased in the diet. The maintenance need for Thr represented 5.5% of the total need for Thr. The data suggest that efficiency of Thr utilization is constant at all levels of Thr intake between 5 and 95% of the level required for maximal weight gain and feed efficiency.

Analysis of Variance↗

PubMed1997

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.

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.

Animal Feed↗

PubMed1997

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.

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.

Analysis of Variance↗

PubMed1997

Effect of 1,25-dihydroxycholecalciferol, cholecalciferol, and fluorescent lights on the development of tibial dyschondroplasia and rickets in broiler chickens.

Experiments were conducted to determine whether dietary 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] will alleviate a cholecalciferol deficiency induced by low dietary cholecalciferol and no fluorescent lighting and to determine cholecalciferol requirements as influenced by fluorescent lighting or 1,25-(OH)2D3. In each study, nutritionally complete basal diets were fed to broiler cockerels from 1 to 16 d of age. Experiment 1 had a 2 x 2 x 2 factorial arrangement of treatments with 1,25-(OH)2D3 at 0 and 10 micrograms/kg, cholecalciferol at 2.75 and 27.5 micrograms/kg, and fluorescent lights on or off. Experiments 2 to 4 had four levels of dietary cholecalciferol (0, 5.0, 27.5, and 50.0 micrograms/kg) and fluorescent lights on or off (Experiment 2) or 1,25-(OH)2D3 at 0 and 10 micrograms/kg (Experiments 3 and 4). In Experiment 1, fluorescent lighting increased bone ash, and decreased the incidence and severity of rickets at 2.75 micrograms/kg cholecalciferol and 0 microgram/kg 1,25-(OH)2D3 and reduced the severity of TD at both levels of cholecalciferol and 0 microgram/kg 1,25-(OH)2D3. In all cases 1,25-(OH)2D3 improved bone ash. The metabolite also decreased the incidence and severity of TD at both cholecalciferol levels with lights off and decreased the incidence and severity of rickets at 2.75 micrograms/kg cholecalciferol and lights off. In the absence of fluorescent lighting and 1,25-(OH)2D3 27.5 micrograms/kg cholecalciferol reduced the incidence and severity of rickets to levels equivalent to those produced by either fluorescent lighting or 1,25-(OH)2D3 alone (Experiments 2, 3, and 4). However, even 50.0 micrograms/kg cholecalciferol was not as effective as fluorescent lights or 1,25-(OH)2D3 in reducing the incidence and severity of TD.

Animals↗

PubMed1996

Maintenance requirement for valine and efficiency of its use above maintenance for accretion of whole body valine and protein in young chicks.

Experiments were conducted with chicks during the period 10-20 d posthatching to assess valine accretion and protein accretion as a function of incremental valine intakes between 5 and 95% of its ideal level (requirement for maximal growth). Chemically defined crystalline amino acid diets were fed, and amino acids other than valine were maintained at minimized excess levels as valine was increased. With dietary valine concentrations representing 5, 10, 40, 55, 70 and 95% of the ideal level, weight gain (r2 = 0.98), protein accretion (r2 = 0.98) and valine accretion (r2 = 0.99) increased linearly (P < 0.01) as a function of valine intake. Slope of the valine accretion curve was 0.73 +/- 0.02, and there was no indication of decreased valine utilization as valine intake increased to 95% of its required level for maximal growth. Using the linear regression equation, i.e., valine accretion (Y) regressed on valine intake (X), the maintenance valine requirement (X at Y zero) was 18.4 mg/d or 48.8 mg/d per kg body weight3/4. Whole body valine was 4.72 g/100 g whole body protein accreted and was constant at all levels of valine intake. At zero protein accretion, however, valine accretion was negative (-3.8 mg/d). Thus, the valine requirement for zero valine accretion (48.8 mg/d per kg(3/4) was higher than the valine requirement for zero protein accretion (32.4 mg/d per kg3/4). In a subsequent experiment, also involving whole body valine and protein accretion, valine doses of 40, 55 and 70% of ideal were compared using amino acid-balanced diets (amino acids other than valine at 55, 70 and 85% of ideal levels, respectively) or imbalanced diets (amino acids other than valine at a constant 100% of their ideal levels). Straight-line (P < 0.01) valine and protein accretion responses occurred, but slope of the response curves (accretion vs. valine intake) was lower in the imbalanced series than in the balanced series. The results of these studies suggest a constant utilization above maintenance of absorbed valine over a wide range of valine intake.

Analysis of Variance↗

PubMed1996

Efficacy of a lysine-tryptophan blend for growth of chicks.

Two chick experiments were conducted to compare the growth-promoting efficacy as well as the toxicity of a new source of L-tryptophan and L-lysine, Tryptosine (16.1% tryptophan, 56.3% lysine). A corn-feather meal-soybean meal basal diet was made singly deficient in either lysine or tryptophan, and graded doses of lysine or tryptophan from either Tryptosine or feed-grade sources of lysine and tryptophan were supplemented. Linear (P < .01) weight gain responses occurred, and responses to lysine or tryptophan in Tryptosine were similar to those obtained with equal doses of lysine or tryptophan provided by feed-grade sources of L-lysine.HCI or L-tryptophan. The toxicity trial involved additions of 1, 2, or 4% lysine with .29, .58, or 1.16% tryptophan to a lysine- and tryptophan-adequate corn-soybean meal diet. Both amino acids were provided as either Tryptosine or as feed-grade sources of lysine and tryptophan. Weight gain and feed intake were reduced in a linear fashion (P < .01) as levels of the two excess amino acids increased. The decreases caused by Tryptosine were similar to those caused by equivalent levels of excess feed-grade lysine and tryptophan.

Animals↗

PubMed1996

Effect of dietary 1,25-dihydroxycholecalciferol level on broiler performance.

Studies were conducted to evaluate the level of dietary 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] required to decrease the incidence of tibial dyschondroplasia (TD) in male broilers at 3 and 5 wk of age. The birds were reared in floor pens with wood shavings and fed a corn-soybean meal diet supplemented with 0, 3, 6, or 9 micrograms/kg 1,25-(OH)2D3. The diet contained, by averaged analyses, 0.73% calcium, 0.74% total phosphorus, and 0.22% phytate phosphorus. There was no treatment effect on body weight or gain: feed at either age. The incidence and severity of TD and the percentage of severe lesions were decreased and bone ash was increased by 6 micrograms/kg 1,25-(OH)2D3 at 3 wk of age. At 5 wk of age, the incidences of TD and severe lesions were decreased when 6 micrograms/kg 1,25-(OH)2D3 was fed. Bone ash was increased by this level in one of the two experiments. Plasma calcium was increased at 5 wk when 9 micrograms/kg 1,25-(OH)2D3 was fed, but there was no treatment effect on plasma dialyzable phosphorus or 1,25-(OH)2D3. The results indicate that 6 micrograms/kg 1,25-(OH)2D3 is effective for decreasing TD under practical rearing conditions.

Animals↗

PubMed1996

Effects of phytase and 1,25-dihydroxycholecalciferol on phytate utilization and the quantitative requirement for calcium and phosphorus in young broiler chickens.

Three experiments were conducted to determine the effects of supplementing 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] and a commercial phytase product on Ca and P requirements of 0- to 21-d-old broiler males. These experiments were conducted with four levels of dietary Ca and P in corn-soybean diets with and without supplementation of 5 micrograms/kg of 1,25-(OH)2D3, 600 units/kg of phytase, and the combination of these supplements. The results show that these levels of phytase and 1,25-(OH)2D3 can replace up to 0.1% of the inorganic P for criteria such as BW, bone ash, and plasma P. Both supplements increased phytate P retention, whereas higher levels of Ca and P decreased phytate P retention. The addition of 1,25-(OH)2D3, but not phytase, reduced Ca requirements and decreased the incidence of tibial dyschondroplasia. The combination of these levels of phytase and 1,25-(OH)2D3 replaced 0.2% inorganic P for criteria such as BW, bone ash, and P rickets. Total dietary P requirements are estimated to be between 0.55 and 0.60% at the levels of phytase and 1,25-(OH)2D3, listed above, or 0.45% when the combination is added. The Ca requirements are estimated to be 0.77% when 1,25-(OH)2D3 is added to the diet and 0.9 to 0.95% when phytase is added.

6-Phytase↗

PubMed1996

Additive effects of 1,25-dihydroxycholecalciferol and phytase on phytate phosphorus utilization and related parameters in broiler chickens.

Two experiments were conducted to compare the effects of supplementation with 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] and a commercial phytase on P utilization by broiler males. Experiment 1 was conducted with three levels of total dietary P (0.45,0.55, and 0.65%) in corn-soybean meal diets supplemented with 5 micrograms/kg of 1,25-(OH)2D3, 600 units/kg of phytase, or the combination of these supplements in a factorial arrangement from 0 to 21 d in battery brooders. A second experiment was conducted with a similar design except that it was carried out in floor pens for a period of 35 d. In Experiment 1, maximal BW was obtained at 0.65% P in chicks receiving the basal diet, 0.55% P in chicks receiving phytase or 1,25-(OH)2D3, and 0.45% P in chicks fed both supplements. Bone ash for chicks receiving the basal, phytase, 1,25-(OH)2D3, and combination treatments at 0.45% total dietary P were 26.6, 34.9, 35.1, and 38.8%. There were significant interactions between phytase and 1,25-(OH)2D3 for BW, bone ash, and incidence of rickets. Similar results were noticed in Experiment 2, with the exception that 1,25-(OH)2D3 had little influence on BW from 0 to 3 wk, likely due to slightly higher dietary P. From 3 to 5 wk, BW and bone ash were increased by each supplement and further increased by their combination. These interactions suggest different mechanisms of action for these supplements in influencing phytate P utilization.

6-Phytase↗

PubMed1995

The folic acid requirements of starting broiler chicks fed diets based on practical ingredients. 2. Interrelationships with dietary methionine.

Two experiments were conducted to determine the effects of dietary supplemental folic acid and methionine on the performance of starting broiler chicks for 18 d. Four levels of dietary folic acid (.24, .54, 1.14, and 2.34 mg/kg) and four levels of dietary methionine (.45, .53, .61, and .69%) were fed in a factorial design. There were three replicates of eight chicks each per each treatment. The basal diet was based on corn, isolated soybean protein, meat and bone meal, and fish meal. It contained adequate amounts of all nutrients except methionine and folic acid. Increased growth was observed in chicks fed the basal diet supplemented with either folic acid or methionine. Total dietary folic acid and methionine plus cysteine requirements for maximum growth were estimated to be 1.80 mg/kg and .85% in Experiment 1 and 1.47 mg/kg and .87% in Experiment 2, respectively. There were interactions between dietary folic acid and methionine on weight gain in both experiments. Chicks fed the diet containing 2.34 mg folic acid/kg tended to have depressed growth, as in previous experiments. There was a significant linear feed conversion response to folic acid in Experiment 1 and to methionine in Experiment 2. There were both linear and quadratic liver folic acid responses to dietary folic acid in both experiments. There was no indication that dietary methionine had any effect on liver folic acid content. No differences in bone ash, hemoglobin, hematocrit, or incidence of tibial dyschondroplasia were detected due to methionine or folic acid supplementation.

Animals↗

PubMed1995

Effects of dietary calcium and 1,25-dihydroxycholecalciferol on the development of tibial dyschondroplasia in broilers during the starter and grower periods.

Two experiments were conducted to determine whether dietary 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] can prevent tibial dyschondroplasia in broiler chickens throughout the growing period when withdrawn from the grower diet. The birds were reared in floor pens with pine shavings to 6 wk in Experiment 1 and 5 wk of age in Experiment 2. Calcium was fed at .65 or 1.00% and 1,25-(OH)2D3 was fed at 0 or 5 micrograms/kg to 3 wk of age. Half the birds consuming 1,25-(OH)2D3 were then fed 0 microgram/kg until the end of the experiments. The higher level of calcium decreased the incidences of tibial dyschondroplasia and severe lesions and increased bone ash. Dietary 1,25-(OH)2D3 increased bone ash at both levels of calcium at 3 wk and the end of the experiments when supplemented for the duration of the studies. When 1,25-(OH)2D3 was fed, tibial dyschondroplasia was reduced in Experiment 2 only at 3 wk. Tibial dyschondroplasia was decreased at 5 wk in Experiment 2 when .65% calcium was fed with or without 1,25-(OH)2D3 from 3 to 5 wk of age. There were no treatment effects on plasma calcium, dialyzable phosphorus, or 25-hydroxycholecalciferol. Plasma 1,25-(OH)2D3 was decreased at 3 and 5 wk in Experiment 2 when 1.00% calcium was fed. The results of Experiment 2 suggest that 1,25-(OH)2D3 can prevent tibial dyschondroplasia caused by inadequate calcium when fed for only 3 wk. The bone ash observed when 1.00% dietary calcium is fed is equal to that obtained when 5 micrograms/kg 1,25-(OH)2D3 is fed with .65% calcium for the entire growout period.

Age Factors↗

PubMed1994

Effects of ascorbic acid and 1,25-dihydroxycholecalciferol on alkaline phosphatase and tibial dyschondroplasia in broiler chickens.

1. The effects of graded amounts of dietary ascorbic acid with or without 10 micrograms/kg dietary 1,25-dihydroxycholecalciferol on performance, blood and bone variables were measured in broiler chicks. 2. 1,25-Dihydroxycholecalciferol prevented the tibial dyschondroplasia and rickets caused by feeding a low calcium diet. Gain:food was decreased, but body weight was not affected by feeding 10 micrograms/kg 1,25-dihydroxycholecalciferol. Phytate phosphorus retention was increased by dietary 1,25-dihydroxycholecalciferol. 3. Dietary ascorbic acid did not influence the incidence of tibial dyschondroplasia, but did reduce the incidence of rickets at a dietary concentration of 250 mg/kg. Gain:food was increased when 250 or 500 mg ascorbic acid/kg diet were added along with 10 micrograms/kg 1,25-dihydroxycholecalciferol in one of two experiments. 4. Alkaline phosphatase activity and plasma 1,25-dihydroxycholecalciferol were not affected by the dietary treatments. Plasma 25-hydroxycholecalciferol concentration was decreased by dietary 1,25-dihydroxycholecalciferol. 5. Ascorbic acid had no synergistic effects with 1,25-dihydroxycholecalciferol on the blood and bone variables investigated in broiler chickens at the dietary concentrations of 1,25-dihydroxycholecalciferol used in this work.

Alkaline Phosphatase↗

PubMed1994

Quantitative requirement for cholecalciferol in the absence of ultraviolet light.

Studies were conducted to determine the basic requirement of the bird for cholecalciferol in the absence of ultraviolet light by utilizing filter sleeves on fluorescent lights in the room and brooder. In Experiment 1, some pens were fitted with filter tubes and some lights were turned off. All the birds received a cholecalciferol-deficient diet. Birds with ultraviolet light excluded grew slowly, developed rickets (95%), had low plasma calcium, and low bone ash (27%); whereas birds exposed to the fluorescent light had normal growth and plasma calcium, slightly low bone ash (38%), and some rickets (12%). Experiments 2 and 3 were conducted to determine the amount of cholecalciferol that must be added to the diet under conditions in which ultraviolet light was excluded. In Experiment 2, the highest level of cholecalciferol fed was 400 ICU/kg. This level was not sufficient to permit the chickens to have weight gain or bone ash equal to the birds receiving the ultraviolet light. The birds receiving 400 ICU/kg of diet also had a 77% incidence of rickets compared with 20% for the birds receiving ultraviolet lights. In Experiment 3, when birds received 800 or 1,600 ICU/kg of cholecalciferol in the diet, they grew and were comparable to those receiving ultraviolet light for the criteria measured.

Animals↗

PubMed1994

Effect of early castration on body weight, muscle growth, and bone characteristics of male Nicholas strain turkeys.

Body weight of male Nicholas strain turkeys, castrated at 8 to 10 d of age, averaged .60, 2.20, 5.26, 8.26, and 10.83 kg at 3, 6, 9, 12, and 15 wk of age, respectively. These weights did not differ significantly from those of sham-operated control birds, but were significantly less than those of unoperated controls at 12 and 15 wk of age. Pectoralis major weights of 15-wk-old castrated turkeys were not significantly different than the sham-operated controls, but were less than those of intact controls. Pectoralis weights, expressed as a percentage of BW, did not differ among these groups. There were no differences in tarsometatarsal lengths, weight, or percentage ash among the groups. The incidence of tibial dyschondroplasia ranged from 66.7 to 80.0%, with average scores ranging from 1.00 to 1.42, with no differences among groups. Plasma testosterone concentrations of unoperated and sham-operated controls averaged .16 and .26 ng/mL at 15 wk, whereas concentrations in 7 of 12 castrates were undetectable and amounts in the other 5 castrates averaged .03 ng/mL.

Animals↗

PubMed1994

Effect of genetic strain, calcium, and feed withdrawal on growth, tibial dyschondroplasia, plasma 1,25-dihydroxycholecalciferol, and plasma 25-hydroxycholecalciferol in sixteen-day-old chickens.

Four experiments were conducted to study the effects of genetic strain, dietary Ca level, and feed withdrawal on growth, feed efficiency, tibia bone ash, tibial dyschondroplasia (TD), and plasma 1,25-dihydroxycholecalciferol [1,25(OH)2D3] and 25-hydroxycholecalciferol [25(OH)D3]. Experiment 1 used five strains and Experiments 2 to 4 used three broiler strains. A TD-inducing basal diet was used in each experiment. In Experiment 3, the birds were fed .60 or .95% dietary Ca, and in Experiment 4 the birds were fed the basal diet and were fed or deprived of feed for 8 h daily. In Experiment 1, Athens-Canadian Randombred and Single Comb White Leghorn chicks did not develop TD. In birds fed the basal diet alone, Peterson x Hubbard chicks had a significantly higher incidence of the most severe TD lesion than two other broiler strains in each experiment and were significantly lighter in BW in two of the four experiments. Of the three broiler strains, the incidence and average lesion score of TD was significantly higher in Peterson x Hubbard birds in Experiment 2 and was numerically highest in the other three experiments. In birds fed the basal diet, Peterson x Hubbard birds had significantly higher plasma 1,25(OH)2D3 in two of the four experiments. Both feed deprivation and .95% Ca increased bone ash and decreased the incidence and severity of TD. There were no significant differences in plasma 1,25(OH)2D3 among strains of birds deprived of feed or fed .95% Ca. In three of the four experiments, high plasma 1,25(OH)2D3 in Peterson x Hubbard birds was associated with an increase in the incidence and severity of TD.

Animals↗