At present, we see broiler chickens weighing more than 2.4 kg at 42 days of age and layers producing about 320 eggs in a 52-week laying period. But the rapid change in genetic potential of the chicken has made them prone to several metabolic diseases like ascitis, sudden death syndrome, skeletal abnormalities, and other conditions during the growing phase. Fast growth rate in broilers is associated with development of tibial dyschondroplasia (TD). Reducing the growth of broilers can minimize the incidence of TD, but this may not be plausible on economic ground.
The intensive poultry operation is concentrated in relatively small areas in many parts of the world. This is posing potential environmental problems due to the possible threat of contaminating the ground water and surface water bodies through leaching of unutilised P (phytate) into the environment.
To combat these problems and also to sustain the production of the birds to their genetic potential, well-balanced but economical nutrition is an utmost priority in present day poultry production. Present nutrient requirements of commercially grown birds are widely different from the recommended values once used. The nutrient dynamics, particularly calcium (Ca) and phosphorus (P), are very fast in chickens and any imbalance in these minerals leads to severe economic loss due to reduced growth, poor carcass quality, reduced egg production, broken eggs and lameness.
Besides enhancing utilisation of bound phytate phosphorus and development of cell-mediated immunity in chicken, cholecalciferol (CC) plays a vital role in utilisation of dietary calcium (Ca) and phosphorus (P).
Dietary CC will be converted into 1,25-dyhydroxy CC (1,25-DHCC), which is essential for synthesis of calcium-binding protein in the intestines and thereby increased absorption of Ca and P through the gut. Both hypophosphatemia and hypocalcaemia stimulate the synthesis of 1,25-DHCC. There is substantial evidence that phytase and other phosphatases present in the intestinal mucosa of chicken and their activities were reported to increase with CC supplementation in the diet. Metabolites of CC (25-HCC or 1,25-DHCC) are also known to enhance phytin P utilisation. Therefore, the utilisation of phytin-bound minerals (Ca, P, Mn, Fe, Cu, Zn, etc.) was reported to be enhanced with supplementation of CC or its metabolites in the diet. CC is necessary for maturation of pro-monocytes to macrophages and proper functioning of the macrophages (phagocytic and cytotoxic activity). Therefore, CC deficiency leads to poor cell mediated immunity in chicks.
Impact of other factors
The requirement of CC in chicken diets largely depends on the levels and the ratio of Ca and P and concentration of phytate P in the diet. Concentrations of vitamin C, vitamin A, supplemental fat, nature of the light, and other factors are also known to modify the CC requirements in chicken. Also, the requirement for CC is higher in diets contaminated with mycotoxins.
Wider Ca to P ratios (Ca:P) lead to the formation of calcium phosphate, which is not soluble in the gut and gets excreted. This leads to deficiency of both Ca and P and pollutes the environment when the litter is used as manure for crop production. Widening Ca:P were reported to reduce the activity of mucosal phytase up to 15 percent. The ill effects can be negated by supplementation of higher concentrations of CC in the diet. Increasing CC levels beyond 1500 ICU/kg diet increased the bone ash content at a wider ratio of Ca:NPP (6.3:1).
Several reports indicated that supplementation of either CC or its metabolites in low Ca-to-inorganic-P (iP) ratio diets improved the utilisation of phytate P. CC was known to increase the activity of intestinal phytase in chicken. However, the efficiency of CC in improving the utilisation of phytin P is greatly influenced by dietary concentrations of Ca and P. With wider Ca:iP, Ca suppress the P availability through complex formation and by inhibiting the intestinal phytase activity. At sub-optimal levels of Ca and iP in the diet, CC elicits maximum influence on phytin utilisations. At lower concentrations of Ca:aP (0.4:0.2 percent), the body weight gain increased progressively with the level of CC in the diet (300 to 1200 ICU/kg). Since the absorption of Ca is enhanced with CC supplementation, lower quantities of Ca is available in the gut, which may not interfere with the utilisation of P and phytate from dietary sources. But such improvement in growth was not observed with the vitamin supplementation at higher levels of these minerals (>0.6 and 0.3 percent, Ca:iP, respectively) in the diet (See Fig 1). The improvement in growth of broilers fed diets containing sub-optimal Ca:iP levels appear to be increased phytate P availability. Further, the data suggested lower requirements of CC (300 ICU/kg) in diets containing higher or optimum levels of Ca and iP in diet.
Vitamins C and A
Vitamins C and A help in conversion of CC into 1,25DHCC (a metabolic active form) by activating 25-HCC 1-hydroxylase. Therefore, higher concentrations of vitamin C (250 to 3000mg/kg diet) increased bone mineralisation and reduced the incidence of rickets in birds. During thermal stress, synthesis of ascorbic acid and conversion of CC to 1,25DHCC are reduced. Therefore, increasing the concentrations of CC higher than the recommended levels during summer is essential. Higher dietary levels of vitamin A (45000 IU/kg) interfere with the utilisation of CC and its metabolites in chicken.
Higher levels of dietary fat
Higher levels of fat in the diet (9 percent) decreases Ca retention and bone calcification. The depressing effects of higher levels of dietary fat may be due to the formation of Ca and Mg soaps, which are not absorbed through the gut and lead to Ca deficiency. Supplementation of CC to a high fat diet (7.9 percent) was reported to increase the tibia ash content.
Light influences requirements
The nature of light provided in the poultry shed influences the requirement of CC for chicken. Requirement of the vitamin is lower for chicks exposed to UV rays by use of fluorescent bulbs compared to those not exposed to UV rays (incandescent bulbs).
A higher incidence of TD was reported in broilers fed adequate levels of Ca and CC (400 ICU/kg diet) in absence of fluorescent light. In absence of UV rays, the requirement of CC for optimum growth and leg health is much higher (800 to 1500 ICU/kg) in diets containing the recommended levels of Ca and iP (1.1 and 0.61 percent, respectively).
Mycotoxins reduce utilisation
Aflatoxin in chicken diets is known to reduce the utilisation of CC, by interfering in conversion of CC to its metabolites. Fusarium toxin causes changes in the basic steroid structure of CC, which reduces its availability. The ill effects of aflatoxin (2500 ppb) on growth and haemoricrit were partially corrected with higher levels of CC (4400 ICU/kg) in the diet.
Age and breed influences
In newly hatched chicks (up to 14 days of age), the enzyme required for conversion of CC to 25-HCC (CC 25 hydroxylease) is not adequate. Therefore, during this juvenile phase, the chick primarily depends on the maternal supply of the vitamin through yolk. Chicks from parents fed deficit levels of CC exhibit lameness irrespective of CC concentration in the chick diet. Further, the activity of 25 (OH) 1-hydroxylase in the kidney was reported to be depressed and degradation of 1,25-DHCC increased as the age of the bird increases after peak egg production (45 to 50 weeks of age).
Therefore, supplementation of CC metabolites or higher levels of CC in aged layer diets improved eggshell quality. High incidence of TD in certain breeds was attributed to poor utilisation of CC.
Metabolites of CC
Cholecalciferol will be converted into 25-HCC initially and, depending on the status of Ca and P in serum, 25-HCC will be further hydroxylated into 1,25-DHCC. The former is a predominant form of metabolite in the circulation, while the latter is the active form of the vitamin, which takes part in metabolism of Ca, P and other functions of the vitamin. Absorption of CC metabolites (25-HCC) is considerably higher (83.6 percent) than that of CC (66.5 percent) in chicks and is 8 to 12 times more effective than CC in prevention of skeletal disorders. Certain plant leaves also contain the CC metabolites. Leaves of Cestrum diurnum contained higher concentrations of free metabolites of CC (25-HCC, 1,25-DHCC) compared to the parent compound, i.e. CC.
The CC metabolites having hydroxyl group at 1 position i.e. 1-H CC, 1,25 and 1,24R-DHCC, were reported to prevent the development of TD and increased bone ash content. Similarly, replacing CC with 25-HCC on a weight basis (3000 ICU/kg) significantly decreased the incidence of TD from 65 to 10 percent in broiler chickens fed a diet with recommended concentrations of Ca and P. Metabolites of CC (25-HCC, 1,25-DHCC) enhance the activity of intestinal phytase in chicken and are known to increase the availability of P and Ca from vegetable feed ingredients. However, proper mixing is essential when the metabolites are used in poultry diets, as these compounds are about 100 times more toxic than CC.
The requirement of CC in chickens depends on several factors as discussed. The vitamin requirement is generally less in diets containing adequate levels of Ca, and increases (800 to 7920 ICU/kg) as the levels of Ca and iP increase in the diet.
At adequate levels of Ca (1 percent) and iP (0.49 percent), 200 ICU CC/kg diet was reported to be adequate for maximum growth. The requirement of CC for bone ash content is higher compared to body weight gain.
Studies conducted at this laboratory suggest the possibility of reducing the dietary levels of Ca and iP to 50 percent of the recommended levels by increasing concentrations of supplemental CC from 200 to 3600 ICU/kg in the diet without affecting weight gain, feed efficiency, leg score and bone mineralisation (Table 1). This approach could save the costs of feed to the extent of $3.5/T as well as considerably reducing the P excretion.
Development of TD is the characteristic of CC deficiency in broiler chickens. As conversion of CC to 1,25-DHCC is not effective in young, rapidly growing broilers, the incidence of TD is higher. For each increase of 400 ICU 25-OH-CC/kg fed, up to 2800 ICU/kg, it was predicted to reduce the incidence of TD by about 1 to 2 percent in broilers.
It is concluded that 25-HCC may be an effective practical means of improving broiler leg health by alleviating the incidence and severity of TD. Dietary supplementation with 1,25-DHCC showed consistently positive results in alleviating TD by stimulating chondrocyte differentiation.
The toxic effects of CC on the broiler diet depend on the level of Ca in the diet. As the level of Ca increases, lesser levels of CC are necessary to produce toxic effects in chicken. The risk of CC toxicity is very low in practical poultry diets. Surfeit levels of CC up to 50,000 ICU/kg did not exhibit any toxic effects on broiler chicks, even in diets containing the recommended levels of Ca and P. A level of 138,000 ICU CC /kg diet was required to produce renal calcification. Metabolites of CC are more toxic than the parent compound. For example, 25-HCC is 5 to 10 times more toxic than CC. It has been shown that 1,25-DHCC at 200ICU/kg in diets having recommended levels of Ca depressed growth.
Cholecalciferol is an essential fat-soluble vitamin and plays a predominant role in metabolism of dietary Ca and P by increasing synthesis of Ca-binding protein and increasing the activity of intestinal mucosal phytase, respectively.
Enhanced absorption of Ca due to cholecalciferol reduces the Ca concentration in the gut, which in turn enhances utilisation of phytin phosphorus through increasing mucosal phytase. Requirement of supplemental phosphorus can be decreased considerably with cholecalciferol supplementation, which also minimizes excretion of phosphors into the environment.
Metabolites of CC are more efficient compared to the parent compound in minimizing rickets and tibial dyschondroplacia in broilers. The requirement of the vitamin also depends on calcium to phosphorus ratios, concentration of phytate, vitamin C, vitamin A, dietary fat, nature of light, fungal toxins, age and breed of the bird. In practical broiler diets, a minimum of 3600 ICU cholecalciferol/kg diet is required for optimum growth and bone mineralisation.