White Leghorn pullets were fed standard laying rations supplemented with 0.0%, 0.05%, and 0.1% levels of dietary caffeine. There was no statistical difference in fertility among the three groups. Embryonic loss in eggs from pullets fed 0.05% caffeine was between values previously reported for 0.0% and 0.1% dietary caffeine. This suggests that embryonic mortality increases as levels of caffeine are increased in the diet up to 0.1%.
Ro 5–0013 is a new broad spectrum coccidiostat and antibacterial containing sulfadimethoxine, N′-(2,6-dimethoxy-4-pyrimidinyl) sulfanilamide and potentiator, 2,4 diamino-5-(4,5-dimethoxy-2-methylbenzyl) pyrimidine, hereafter referred to as the potentiator, in a ratio of 5:3. Sulfadimethoxine alone has been reported to be highly effective, therapeutically, against all pathogenic species of coccidia in chickens (0.05%) and turkeys (0.025%) when administered in the drinking water (Mitrovic and Bauernfeind, 1967) and efficacious in the prevention of turkey coccidiosis at 0.0125% in the feed (Mitrovic, 1968). Mitrovic (1967) found that sulfadimethoxine was also effective in the therapy of fowl cholera in chickens (0.05%) and turkeys (0.025%) and infectious coryza in chickens (0.05%) when administered in the drinking water. Combining sulfadimethoxine and the potentiator, a folic acid antagonist, in a 5:3 ratio (Ro 5–0013) results in enhanced broad spectrum coccidiostatic and antibacterial activity when fed continuously to broilers at 0.02% and replacement birds at 0.01% (Mitrovic et al.,…
LUX (1954) has shown that the activity of sulfonamides against E. tenella was enhanced when used in combination with members of a class of pyrimidine and triazine compounds. Notable among these were 2,4-diaminopyrimidines. Joyner and Kendall (1955, 1956), Horton-Smith et al. (1960), Ball (1964) and Clarke (1962, 1964) not only confirmed the above reported findings, but expanded them to include other Eimeria species. It is known today that sulfonamide-potentiator mixtures interfere with folic acid, dihydrofolic acid and tetrahydrofolic acid metabolism in sequential biogenic fashion. The resulting beneficial therapeutic responses are the enhancement in activity, lower drug concentrations, reduction in toxicity and nil drug resistance. Mitrovic and Bauernfeind (1967) and Mitrovic (1967, 1968) have reported on sulfadimethoxine [(N’-(2,6-dimethoxy-4-pyrimidinyl) sulfanilamide)]-anticoccidial and antibacterial activity in fowl when used alone. In evaluating the newly synthesized 2,4-diamino-5-substituted benzylpyrimidines in combination with sulfadimethoxine against bacterial and protozoal laboratory infections, a high degree of activity was exhibited . . .
Lasalocid (.0125%) alone and combined with roxarsone (.005%) was evaluated for its effect on lesion reduction and oocyst suppression in thirty-five controlled replicated battery experiments, using in excess of 6200 broiler chickens. The chickens were inoculated with field isolates containing predominantly Eimeria tenella species. Lasalocid (.0125%) used alone exhibited a high degree of anticoccidial activity. Lasalocid (.0125%) fed in combination with roxarsone (.005%) showed, in addition to high anticoccidial activity, a further reduction in gross lesion (P<.01) and oocyst production (P<.05) over lasalocid used alone.
The ability of selected anticoccidial drugs to inhibit the colonization of day-old male broiler chicks (Cornish Rocks) by Escherichia coli 0157:H7, strain 932 was examined. Chicks were challenged with 1.8 × 10⁹E. coli 0157:H7 on Day 1, and fed diets supplemented with three selected anticoccidial drugs; monensin, nicarbazin, or robenidine. The cecal and colon fecal contents of the chicks were removed on Day 7, 14, and 21 postinoculation and examined for the concentration of E. coli 0157:H7 per gram of contents. Monensin effectively reduced cecal and colon colonization of the chicks by E. coli 0157:H7. By Day 7, there were significant reductions in the bacterial population of the cecal contents of chicks receiving the monensin-medicated feed, and by Day 21 no E. coli 0157:H7 was recovered from the cecal and colon contents. The bacterial counts in the colon contents of the nicarbazin- and robenidine-medicated and unmedicated chicks were significantly higher than the monensin-treated chicks. Bacterial populations in the colon contents were high only when there were high bacterial concentrations in the cecal contents.
Control diets, and diets containing 4% 1,3-butanediol (BD), 8% BD, 4% 1,2-propanediol (PD) and 8% PD were offered ad libitum to broilers from 1 to 28 days of age. Body weight gain and feed intake were recorded, and plasma metabolites and liver glycogen were measured. When compared to the control diet, the synthetic compounds depressed (p less than 0.01) growth at the 4% level, but the effect was more pronounced (p less than 0.01) at the 8% level. The test compounds had no effect (p less than 0.05) on the efficiency of feed utilization. Four percent BD elevated (p less than 0.01) plasma beta-hydroxybutyrate and acetoacetate concentrations, and the ratio of beta-hydroxybutyrate to acetoacetate. The influence was more pronounced at the 8% level; PD did not affect (p greater than or equal to 0.05) ketone body concentrations. Neither BD, nor PD caused changes (p greater than or equal to) in plasma glucose, free fatty acids, cholesterol, or liver glycogen. Results are discussed with reference to feeding these compounds to monogastric and ruminant animals.
Five sources of corn distillers dried grains in the darkest DDGS source. Apparent and true lysine with solubles (DDGS), which varied in darkness of color, were collected from several processing plants in the Midwestern United States. Sources of DDGS were analyzed for their amino acid and energy contents, measured for color score, and evaluated for TMEn, apparent amino acid digestibility, and true amino acid digestibility. A precision-fed rooster assay was used, in which each DDGS sample was tube fed (25 g) to adult cecectomized roosters, and the excreta were collected for 48 h. The experiment was conducted as a randomized complete block design with 8 replicates. Seven adult roosters (averaging 75 wk of age) were used in each period, with 5 fed the DDGS sources and 2 fasted to estimate basal endogenous amino acid losses. One source (no. 5) was the darkest, 2 sources
Bile Cu accumulation in Cu-depleted chicks fed Cu concentrations between .56 and 1.56 mg Cu/kg (0, .5, or 1 mg supplemental Cu/kg) was used to investigate the effect of microbial phytase at 600 U/kg and 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] at 10 micrograms/kg on Cu bioavailability from dehulled soybean meal (SBM) and cottonseed meal (CSM). The bioavailability of Cu (relative to CuSO4.5H2O, which was set at 100%) in SBM and CSM was 43 and 39%, respectively. Phytase addition (600 U/kg diet) decreased Cu bioavailability in SBM to 21%, but did not affect that in CSM (34%). Copper bioavailability in SBM was not affected by addition of 1,25-(OH)2D3 (10 micrograms/kg diet), but that in CSM was nearly doubled by 1,25-(OH)2D3 supplementation.
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.
An experiment was conducted to determine the influence of adding 4 micrograms/kg of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] to the diet of 68-wk-old commercial egg production-type hens. The addition of the 1,25(OH)2D3 to the diet for 21 days resulted in significantly decreased egg production, egg weight, and feed consumption, and significantly increased plasma P, and bone-breaking load. Specific gravity of eggs, plasma Ca, tibia ash, and fertility and hatchability of eggs were not significantly affected by the addition of 1,25(OH)2D3 to the diet.
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.
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.
Six hundred and sixty 75-wk-old Hy-line® W36 hens were allocated to one of three dietary levels of total phosphorus, .30, .60, or .90%. Birds were fed the diets for 3 days following which blood samples were collected at six different times, 2, 6, 10, 14, 18, and 22 h postoviposition (POP), and analyzed for 1,25-dihydroxycholecalciferol [1,25-(OH)2 D3], total calcium (TCa), ionized calcium (Ca⁺⁺), percentage Ca⁺⁺ to TCa (%Ca⁺⁺/TCa), and phosphorus (P). Plasma TCa and P significantly (P<.001 and .025, respectively) peaked at 10 to 14 h POP. The Ca⁺⁺ and %Ca⁺⁺/TCa significantly (P<.001) decreased during eggshell formation and following completion of the shell (22 h POP) levels returned to resting concentrations. Plasma 1,25-(OH)2 D3 results confirmed the existence and time of a circadian rhythm in laying hens. Peak concentrations of the metabolite occurred at 10 to 14 h POP, which resulted in a quadratic relationship (P<.001). Plasma P decreased with decreasing dietary P and plasma 1,25-(OH)2 D3 increased (P<.025). Feeding low dietary P significantly (P<.001) increased Ca⁺⁺ and %Ca⁺⁺/TCa. Results of feeding various levels of dietary P to laying hens indicate that low P stimulates an increase in plasma 1,25-(OH)2 D3 as well as Ca⁺⁺ and %Ca⁺⁺/TCa, but high P actually suppressed this response.
The research described in this paper relates the changes in serum concentration of calcium, phosphorus, and 1,25-dihydroxycholecalciferol [l,25(OH)2 D3] 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 l,25(OH)2 D3. 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 ≤ .05) concentrations of l,25(OH)2 D3 than flocks mildly affected (12 to 16% incidence). Tibial ash percentages were lower (P ≤ .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. From these studies it is evident that flocks with a high incidence of EOD have significantly lower bone ash and 1,25 (OH)2 D3 compared with mildly affected flocks, and it seems probable that higher systemic concentrations of l,25(OH)2 D3 between 7 to 14 d of age will enhance the ability of broiler chickens to effectively mineralize the cartilaginous growth plates in the appendicular skeleton during early bone maturation.
A series of experiments was conducted to investigate interactions of dietary calcium levels with ultraviolet light, cholecalciferol (D3), 1,25-dihydroxycholecalciferol [1,25-(OH)2D3], dietary protein, and a synthetic zeolite on the development of tibial dyschondroplasia in broilers. A basal diet low in calcium, high in phosphorus and chloride, and known to promote a high incidence of tibial dyschondroplasia was used. The chicks received ultraviolet radiation from fluorescent lights in addition to 1,100 ICU/kg (27.5 μg/kg) of D3 in the basal diet when these were not experimental variables. Regardless of whether the calcium level was low (.65%) or adequate (.95%), the incidence of tibial dyschondroplasia was significantly lower in chicks receiving ultraviolet radiation or dietary vitamin D3 levels well above the required amounts. The addition of 10 μg/kg of 1,25-(OH)2D3 to the diet when calcium levels varied from .45 to .95% resulted in a reduction in the incidence of tibial dyschondroplasia and increased tibial bone ash when dietary protein levels were 18 or 22%. The addition of 1% synthetic zeolite to the diet did not influence the incidence of tibial dyschondroplasia when the diet contained widely varying dietary calcium levels (.65 to 1.81%) and .73% phosphorus.
Seventy-two-week-old Leghorn hens were fed a conventional corn-soybean meal diet, or comparable diets either devoid of all supplemental vitamins, or with additions of 5 microg/kg 1,25-dihydroxycholecalciferol [1,25(OH)2D3], or 100 ppm vitamin C. The diets were fed for up to 30 d, with periodic observation on bone characteristics of selected birds. With a vitamin-deficient diet it took 30 d to realize significant reductions (P < 0.05) in bone breaking strength and these birds had less bone ash as early as 15 d (P < 0.05), although bone calcium content was not affected. Adding 1,25(OH)2D3 to the diet caused an increase in bone breaking strength after 15 d (P < 0.05) in the vitamin-deficient birds, although no difference was seen after 30 d. This increase in bone strength was associated with increase in bone cross-sectional area. Vitamin C generally had little effect on bone characteristics of the bird. These results suggest that there is little bone remodeling of older laying hens in response to short-term feeding of 1,25(OH)2D3 or vitamin C.
White Leghorn hens, age 34 wk, fed 0 to 3 μg/kg of 1,25 dihydroxycholecalciferol (1,25(OH)2D3) as the only source of dietary vitamin D3 with 2.5 or 3.5% calcium failed to achieve normal embryonic survival and hatchability of their fertile eggs. Improved egg production was observed over a 24-wk period as the level of 1,25(OH)2D3 was increased. Eggs of hens fed the vitamin D-deficient diet showed significantly lower (P<.01) egg weight and shell strength with a higher percent of soft shell eggs than those of hens fed l,25(OH)2D3 or vitamin D3. To study the possibility that l,25(OH)2D3 cannot be transferred into the egg yolk, yolks from the hens receiving varying levels of l,25(OH)2D3 and vitamin D3 were fed to day-old chicks. A standard vitamin D3 assay was developed and bone ash was determined on fat-free tibial bone. Significantly lower (P<.01) vitamin D activity per gram of yolk was observed in yolks from hens fed 0 to 3 μg of l,25(OH)2D3 than in yolks of hens fed vitamin D3. These results demonstrate that insufficient 1,25(OH)2D3 is incorporated in the egg yolk to support normal embryonic survival and hatchability. This may be due to a decrease in available receptor sites in the egg yolk or to the inability of l,25(OH)2D3 to cross the vitelline membrane.
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.
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 × 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 × 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 l,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 l,25-(OH)2 D3, TCa, or P in Experiments 1 and 2. In Experiment 3, plasma l,25-(OH)2 D3 and P peaked at 14 h POP, but Ca⁺⁺ was lowest at 14 h POP. Circadian rhythms for plasma l,25-(OH)2 D3, Ca⁺⁺, and P were not affected by SZA. There were no significant effects due to dietary SZA on plasma l,25-(OH)2 D3, TCa, Ca⁺⁺, PCa⁺⁺, nCa⁺⁺, pH, or P. It was concluded that SZA did not influence the synthesis of l,25-(OH)2 D3.
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 [l,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 × 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 × Hubbard birds in Experiment 2 and was numerically highest in the other three experiments. In birds fed the basal diet, Peterson × Hubbard birds had significantly higher plasma l,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 l,25(OH)2D3 among strains of birds deprived of feed or fed .95% Ca. In three of the four experiments, high plasma l,25(OH)2D3 in Peterson × Hubbard birds was associated with an increase in the incidence and severity of TD.
Two experiments were conducted to compare the effects of supplementation with 1,25-dihydroxycholecalciferol [l,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 μg/kg of l,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 l,25-(OH)2D3, and 0.45% P in chicks fed both supplements. Bone ash for chicks receiving the basal, phytase, l,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 l,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.
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.
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.
The effect was studied of 1,25-dihydroxycholecalciferol [1,25-(OH)2D3] at various levels of vitamin D3, with adequate or inadequate dietary calcium, on performance and bone development in turkey poults. Two experiments were conducted. Experiment 1 lasted 16 days and was a 4 × 2 factorial arrangement using a low calcium diet (.7%), with dietary levels of vitamin D3 of 450, 900, 1,800, and 3,600 ICU/kg of diet and with or without 10 μg of dietary l,25-(OH)2D3. Experiment 2 lasted 14 wk and was a 2 × 2 × 2 factorial arrangement with vitamin D3 levels of 900 or 2,700 ICU/kg of diet, calcium levels at 58 or 100% of the National Research Council requirement (which varies with age), and with or without 10 μg/kg of dietary l,25-(OH)2D3. In Experiment 1, increasing levels of vitamin D3 and l,25-(OH)2D3 supplementation significantly increased bone ash. Pairwise contrasts at specific vitamin D3 levels indicated that this effect of l,25-(OH)2D3 was greater at lower levels of vitamin D3. In Experiment 2, the 2,700-ICU level of vitamin D3 decreased the incidence of rickets at 3 wk and partially ameliorated a calcium deficiency, as indicated by an increase in growth at the 2,700-ICU level of vitamin D3 in calcium-deficient diets from 8 to 14 wk. Vitamin D3 by calcium interactions on rickets at 14 wk of age and bone ash at 3 and 14 wk were similar and indicated also that vitamin D3 partially ameliorated a calcium deficiency. In general, the addition to the diet of 1,25-(OH)2D3 increased bone ash and decreased the incidence of rickets in diets deficient in calcium but high in vitamin D3. There is very little evidence in the present study that indicates that 1,25-(OH)2D3 has any effect on tibial dyschondroplasia.
Four hundred 53-wk-old Hyline W36 laying hens were randomly allocated to 10 treatments. The effects of feeding two vitamin D3 metabolites, 1α-hydroxyvitamin D3 [1α-(OH) D3] and 1,25-dihydroxyvitamin D3 [1,25-(OH)2 D3 ], each at five dietary levels (0, .75, 1.50, 3.00, and 4.50 μg/kg of feed) were determined on eggshell quality and tibia strength in commercial laying hens (Experiment 1). In Experiment 2, 1,440 Hyline W36 65-wk-old laying hens were used to determine the effects of four levels of vitamin D3 (0, 500, 1,000, and 1,500 ICU vitamin D3/kg) and three levels of dietary 1,25-(OH)2 D3 (0, .5, and 1.0 μg/kg of feed) on eggshell quality, tibia strength, and egg production. In Experiment 1, neither 1,25-(OH)2 D3 nor 1α-(OH) D3 affected eggshell quality or production criteria. Tibia weight was increased by adding either 1,25-(OH)2 D3 or 1α-(OH) D3. In Experiment 2, 1,25-(OH)2 D3 increased percentage of shell, shell weight, and egg breaking strength when 0 ICU D3/kg was fed but had no effect at higher levels of vitamin D3. Egg production, feed consumption, and egg weight were also increased with supplemental 1,25-(OH)2 D3 when 0 ICU D3/kg was fed. Tibia weight and tibia breaking strength were also increased by adding 1,25-(OH)2 D3 to the diet. The commercial laying hen metabolizes sufficient 1,25-(OH)2 D3 from dietary vitamin D3 to maintain shell quality but not enough to maintain tibia strength.