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5
Vitamins
The term ''vitamin" describes an organic compound distinct from amino acids, carbohydrates, and lipids that is required in minute amounts for normal growth and reproduction. Some vitamins are not required in the diet because they can be synthesized readily from other feed or metabolic constituents, or by microorganisms in the intestinal tract. Vitamins are generally classified as either fat-soluble or water-soluble. The fat-soluble vitamins include vitamins A, D, E, and K. The water-soluble vitamins include the B-vitamins (biotin, choline, folacin, niacin, pantothenic acid, riboflavin, thiamin, B6, and B12) and vitamin C (ascorbic acid).
Vitamins are primarily required as coenzymes in nutrient metabolism. In feedstuffs, vitamins exist primarily as precursor compounds or coenzymes that may be bound or complexed in some manner. Hence, digestive processes are required to either release or convert vitamin precursors or complexes to usable and absorbable forms. The requirements for the individual vitamins at various stages of the life cycle are shown in tables provided in Chapter 10. To meet the deficiencies of vitamins in practical diets, vitamin premixes have been developed and are commonly added to swine diets.
Dietary addition of excess levels of vitamins A and D to the diet has been demonstrated to have toxic effects in swine. In contrast, very few toxicity signs have been reported for the B-vitamins or for vitamins E and K (National Research Council, 1987).
Several recent studies have suggested that National Research Council (1988) levels of one or more of the commonly supplemented B-vitamins (riboflavin, niacin, pantothenic acid, and vitamin B12) are inadequate for maximal performance of newly weaned pigs (Wilson et al., 1991a,b; 1992a,b; 1993) or high lean growing pigs (Stahly et al., 1995). Indeed, additions of these B-vitamins at levels of two to ten times the estimated requirements have tended to improve growth rate or feed efficiency of pigs. However, it is not known what level (above those suggested by the National Research Council in 1988) may be needed. Lindemann et al. (1995) observed a trend toward improved weight gain and feed intake in weanling pigs fed five times National Research Council (1988) levels of commonly supplemented vitamins (including fat-soluble vitamins), but feed efficiency tended to be poorer with the higher levels of vitamin fortification. In a separate study, the same group tested a level of vitamin B12 7.5 times the 1988 standard and observed no positive responses. In most of these previously mentioned studies, combinations of vitamins were added and fortification levels were such that it is not possible to establish revised estimates of requirements for individual B-vitamins. Therefore, the B-vitamin requirements for weanling pigs have not been changed. More research certainly is needed to clarify this issue.
Fat-Soluble Vitamins
Vitamin A
Vitamin A is essential for vision, reproduction, the growth and maintenance of differentiated epithelia, and mucus secretions. Except for its role in vision (Wald, 1968), the exact role of vitamin A in these functions is undefined (Goodman, 1979, 1980). Recent evidence, however, suggests that vitamin A may be involved in gene expression.
Vitamin A nomenclature policy (Anonymous, 1990) dictates that the term "vitamin A" be used for all β-ionone derivatives, other than provitamin A carotenoids, that exhibit the biological activity of all-trans retinol (i.e., vitamin A alcohol, or retinol). Vitamin A is present in animal tissues, eggs, and whole milk, whereas plant materials contain only provitamin A precursors that must be acted upon in the gut or by the liver to form retinol. Both natural vitamin A and synthetic retinol analogs are commonly
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referred to as retinoids. On the basis of rat data, 1 IU of vitamin A equals 0.3 µg of crystalline vitamin A alcohol, 0.344 µg of vitamin A acetate, or 0.55 µg of vitamin A palmitate. Retinol equivalent (RE) is the currently accepted nomenclature used to describe the vitamin activity in foods and feeds. One RE is defined as 1 µg of all-trans retinol.
Pigs are less efficient than poultry or rats in converting carotenoid precursors to vitamin A. This conversion occurs primarily in intestinal mucosa (Fidge et al., 1969). Active carotenoid pigments in corn-soybean meal diets (Wellen-reiter et al., 1969) and their bioactivities relative to all-trans β-carotene (100 percent) are β-zeacarotene (25 percent) and cryptoxanthin (57 percent), as estimated by Petzold et al. (1959), Duel et al. (1945), and Greenberg et al. (1950). Ullrey (1972) calculated, therefore, that the all-trans β-carotene equivalent would be only 52 percent of the chemically determined carotene value. He then calculated that this value for swine would be only 16 percent, based on the fact that pigs are only 30 percent as efficient as rats in converting β-carotene in swine diets to usable vitamin A (Braude et al., 1941). When this value is multiplied by 1,667 IU, which represents the theoretical vitamin A potency of 1 mg of all-trans β-carotene for rats, 1 mg of chemically determined carotene in a corn-soybean meal pig diet would have a calculated potency of 267 IU, or 80 µg of vitamin A alcohol.
Chew et al. (1982) and Brief and Chew (1985) have suggested that β-carotene plays a role in reproduction that is independent of vitamin A. Their studies involving β-carotene injection suggest that elevation of maternal plasma vitamin A or β-carotene may improve embryonic survival, possibly because more uterine-specific proteins are secreted. Dietary addition of β-carotene did not elicit a response. This failure is probably due to the poor absorption of intact β-carotene in the pig (Poor et al., 1987).
Swine are able to store vitamin A in the liver, which makes the vitamin available during periods of low intake. Requirements for vitamin A depend on the criteria evaluated; weight gain is less sensitive than cerebrospinal fluid pressure, liver storage, or plasma levels. For pigs during the first 8 weeks of life, 75 to 605 µg of retinyl acetate/kg of diet is required, depending on the response criteria used (Sheffy et al., 1954; Frape et al., 1959). With growing-finishing pigs, the requirement varies from 35 to 130 µg/kg, when daily gain is used as the criterion, and from 344 to 930 µg/kg, when liver storage and cerebrospinal fluid pressure are used as the criteria (Guilbert et al., 1937; Braude et al., 1941; Hentges et al., 1952a; Myers et al., 1959; Hjarde et al., 1961; Nelson et al., 1962; Ullrey et al., 1965). Presence of nitrite or nitrate in feed or water can increase the vitamin A requirement (Koch et al., 1963; Seerley et al., 1965; Wood et al., 1967; Hutagalung et al., 1968).
The vitamin A reserves of the sow make it difficult to establish requirements. Braude et al. (1941) reported that mature sows fed diets without supplemental vitamin A completed three pregnancies normally; only in the fourth pregnancy did signs of vitamin deficiency appear. Gilts receiving adequate vitamin A levels until 9 months of age, followed by a diet containing no vitamin A, completed two reproductive cycles without signs of vitamin A deficiencies (Hjarde et al., 1961; Selke et al., 1967). Heaney et al. (1963) fed depleted gilts 16, 5, or 2.5 µg of retinyl palmitate/kg body weight daily with no effects on litter size, birth weight, or survival rate. Parrish et al. (1951) suggested that 2,100 IU of vitamin A/day during gestation and lactation was adequate to maintain normal serum and liver concentrations.
Vitamin A deficiency in swine results in reduced weight gain, incoordination, posterior paralysis, blindness, increased cerebrospinal fluid pressure, decreased plasma levels, and reduced liver storage (Guilbert et al., 1937; Braude et al., 1941; Hentges et al., 1952a; Frape et al., 1959; Hjarde et al., 1961; Nelson et al., 1962, 1964).
Gross toxicity signs of hypervitaminosis A include a roughened hair coat, scaly skin, hyperirritability and sensitivity to touch, bleeding from cracks which appear in the skin about the hooves, blood in urine and feces, loss of control of the legs accompanied by inability to rise, and periodic tremors (Anderson et al., 1966). Young pigs fed diets containing 605,000, 484,000, 363,000, or 242,000 µg of retinyl palmitate/kg of diet developed signs of vitamin A toxicity in 16, 17.5, 32, and 43 days, respectively. No signs of toxicity were observed when pigs were fed 121,000 µg of added retinyl palmitate/kg of diet for 8 weeks (Anderson et al., 1966). Wolke et al. (1968) observed lesions in endochondral and intramembranous bone within 5 weeks when pigs were fed these excessive levels of vitamin A.
Vitamin A esters are more stable in feeds and premixes than is retinol. The hydroxyl group as well as the four double bonds on the retinol side chain are subject to oxidative losses. Thus, esterification of vitamin A alcohol does not totally protect this vitamin from oxidative losses. Current commercial sources of vitamin A are generally "coated" esters (1 IU of vitamin A = 0.344 µg of retinyl acetate, or 0.549 µg of retinyl palmitate) that contain an added antioxidant such as ethoxyquin or butylated hydroxytoluene (BHT).
Moisture in premixes and feedstuffs has a negative effect on vitamin A stability (Baker, 1995). Water causes vitamin A beadlets to soften and become more permeable to oxygen. Thus, both high humidity and presence of free choline chloride (which is very hygroscopic) enhance vitamin A destruction. Trace minerals also exacerbate vitamin A losses in premixes exposed to moisture. For maximum retention of vitamin A activity, premixes should be as moisture-free as possible and have a pH above five. Low pH
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causes isomerization of all-trans vitamin A to less potent cis forms and also results in de-esterification of vitamin A esters to more labile retinol (De Ritter, 1976).
Vitamin D
The two major forms of vitamin D are ergocalciferol (vitamin D2) and cholecalciferol (vitamin D3). The action of ultraviolet light on the ergosterol that is present in plants forms ergocalciferol; the photochemical conversion of 7-dehydrocholesterol in the skin of animals forms cholecalciferol. One IU of vitamin D is defined as the biological activity of 0.025 µg of cholecalciferol. Ergocalciferol and cholecalciferol are hydroxylated in the liver to the 25-hydroxy forms. The 25-hydroxy-D3 is further hydroxylated in the kidney to either 1,25-dihydroxy-D3 or 24,25-dihydroxy-D3. Several mechanisms that act according to established criteria for hormones control the synthesis and reactions of the dihydroxylated metabolites; therefore, the dihydroxylated D3 metabolites are viewed as hormones (Schnoes and DeLuca, 1980; Kormann and Weiser, 1984).
Vitamin D and its hormonal metabolites act on the mucosal cells of the small intestine, causing the formation of calcium-binding proteins. These proteins facilitate calcium and magnesium absorption and influence phosphorus absorption. The actions of vitamin D metabolites, together with parathyroid hormone and calcitonin, maintain calcium and phosphorus homeostasis. Braidman and Anderson (1985) have reviewed the endocrine functions of vitamin D.
Bethke et al. (1946) indicated that vitamins D2 and D3 were equally effective in meeting the vitamin D needs of swine. Horst et al. (1982), however, demonstrated that pigs discriminate in their metabolism of the two forms of vitamin D. Additional research is needed in swine to quantify the differences in absorption and utilization of these forms.
The vitamin D2 requirement of the baby pig fed a casein—glucose diet is 100 IU/kg of diet (Miller et al., 1964, 1965). The requirement is higher if isolated soy protein is fed (Miller et al., 1965; Hendricks et al., 1967). Vitamin D deficiency reduces retention of calcium, phosphorus, and magnesium (Miller et al., 1965). Bethke et al. (1946) suggested a minimum requirement of 200 IU/kg of diet for growing pigs. In other studies, however, vitamin D supplementation did not improve weight gain (Wahlstrom and Stolte, 1958; Combs et al., 1966).
No studies of the vitamin D requirement of sows during gestation or lactation have been reported. Weisman et al. (1976), Boass et al. (1977), Noff and Edelstein (1978), Halloran and DeLuca (1979), and Pike et al. (1979) showed that vitamin D is involved in rat reproduction and lactation. Parenteral cholecalciferol treatment of sows before parturition provided an effective means of supplementing pigs with cholecalciferol (via the sow's milk) and its dihydroxy metabolites by placental transport (Goff et al., 1984).
Vitamin D deficiency causes a disturbance in the absorption and metabolism of calcium and phosphorus that results in insufficient bone calcification. In young growing pigs, vitamin D deficiency results in rickets, whereas in mature swine a deficiency causes diminished bone mineral content (osteomalacia). In severe vitamin D deficiency, pigs may exhibit signs of calcium and magnesium deficiency, including tetany. It takes 4 to 6 months for pigs fed a vitamin D—deficient diet to develop signs of a deficiency (Johnson and Palmer, 1939; Quarterman et al., 1964).
Vitamin D toxicity was produced in weanling pigs supplemented with a daily oral dose of 6,250 µg of vitamin D3 for 4 weeks (Quarterman et al., 1964). This level of D3 reduced feed intake; growth rate; and weights of the liver, radius, and ulna. At necropsy, calcification was observed in the aorta, heart, kidney, and lung. Feeding a daily level of 11,825 µg of vitamin D3 to pigs weighing 20 to 25 kg resulted in death in 4 days (Long, 1984). Hancock et al. (1986) reported that there was a reduction in daily gain and feed efficiency in pigs weighing 10 to 20 kg fed a diet containing 550 to 1,100 µg/kg of supplemental vitamin D3/day. Vitamin D3 has been shown to be more toxic than vitamin D2 in a number of species, including swine (National Research Council, 1987). The development of methods to measure vitamin D and its metabolites in plasma has provided insights regarding the possible mechanisms that cause differences in toxicity between vitamins D2 and D3 (Horst et al., 1981; National Research Council, 1987).
Vitamin E
There are eight naturally occurring forms of vitamin E: α, β, γ, and δ tocopherols (Evans et al., 1936; Emerson et al., 1937; Stern et al., 1947) and α, β, γ, and δ tocotrienols (Green et al., 1960; Pennock et al., 1964; Whittle et al., 1966). Of these, D-α—tocopherol possesses the greatest biological activity (Brubacher and Wiss, 1972; Ames, 1979; Bieri and McKenna, 1981). One IU of vitamin E is the activity of 1 mg of DL-α—tocopheryl acetate. The D isomer is more bioactive than the L isomer. On the basis principally of rat bioassay work and using DL-α—tocopheryl acetate as a standard (1 mg = 1 IU), it is calculated that 1 mg DL-α—tocopherol equals 1.1 IU, 1 mg D-α—tocopheryl acetate equals 1.36 IU, and 1 mg D-α—tocopherol equals 1.49 IU of vitamin E. Anderson et al. (1995a), however, suggested that D-α—tocopheryl acetate is utilized more efficiently by pigs than by rats. For young pigs, Chung et al. (1992) reported that 1 mg D-α—tocopherol equals 2.44 IU.
For many years the primary source of vitamin E in feed was the tocopherols found in green plants and seeds. Oxidation, which is accelerated by heat, moisture, rancid
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fat, and trace minerals, rapidly destroys natural vitamin E. Therefore, predicting the amount of vitamin E activity in feed ingredients is difficult. Vitamin E losses of 50 to 70 percent can occur in alfalfa stored at 32°C for 12 weeks; losses of 5 to 30 percent can occur during dehydration of alfalfa (Livingstone et al., 1968). Storage of high-moisture grain or its treatment with organic acids greatly reduces its vitamin E content (Madsen et al., 1973; Lynch et al., 1975; Young et al., 1975, 1978). High levels of dietary vitamin A have also been reported to lower vitamin E absorption (Hoppe et al., 1992), although Anderson et al. (1995b) observed no effects on vitamin E status when growing pigs were fed diets containing 15 times the vitamin A requirement.
During the 1970s, many studies on the vitamin E requirement of swine were conducted. The Agricultural Research Council (1981) and Ullrey (1981) have reviewed the studies. Many dietary factors affect the vitamin E requirement, including levels of selenium, unsaturated fatty acids, sulfur amino acids, retinol, copper, iron, and synthetic antioxidants. Michel et al. (1969) prevented deaths in pigs fed a corn—soybean diet containing 5 to 8 mg of vitamin E/kg and 0.04 to 0.06 mg of selenium/kg by supplementing the diet with 22 mg of vitamin E/kg. Studies of corn—soybean meal diets fed to growing-finishing pigs suggest that 5 mg of vitamin E/kg and 0.04 mg of selenium/kg are inadequate for growing-finishing pigs and may result in deficiency lesions and mortality. In the presence of adequate selenium, however, supplements of 10 to 15 mg of vitamin E/kg of diet prevented mortality and deficiency lesions and supported normal performance (Groce et al., 1971, 1973; Sharp et al., 1972a,b; Ullrey, 1974; Wilkinson et al., 1977b; Hitchcock et al., 1978; Mahan and Moxon, 1978; Meyer et al., 1981). The amount of vitamin E necessary to prevent deficiency signs varies considerably because of variation in dietary levels of selenium (Agricultural Research Council, 1981; Ullrey, 1981), antioxidants (Tollerz, 1973; Simesen et al., 1982), and lipids (Nielsen et al., 1973; Tiege et al., 1977, 1978).
Inclusion of high levels of vitamin E in the diet may increase the immune response (Ellis and Vorhies, 1976; Tiege, 1977; Nockels, 1979; Peplowski et al., 1980; Wuryastuti et al., 1993), although Bonnette et al. (1990) found no evidence of an increased humoral or cell-mediated immune response in young pigs fed high levels of vitamin E.
Vitamin E functions as an antioxidant at the cell membrane level, and it has a structural role in cell membranes. There are vitamin E deficiency diseases that respond to vitamin E, selenium, or antioxidants. Vitamin E deficiency results in a wide variety of pathological conditions. These include skeletal and cardiac muscle degeneration, degenerative thrombotic vessel injury, gastric parakeratosis, gastric ulcers, anemia, liver necrosis, yellow discoloration of fat tissue, and sudden death (Obel, 1953; Davis and Gorham, 1954; Hove and Seibold, 1955; Dodd and Newling, 1960; Grant, 1961; Lannek et al., 1961; Nafstad, 1965, 1973; Nafstad and Nafstad, 1968; Reid et al., 1968; Ewan et al., 1969; Michel et al., 1969; Nafstad and Tollersrud, 1970; Trapp et al., 1970; Baustad and Nafstad, 1972; Sharp et al., 1972a,b; Sweeney and Brown, 1972; Wastell et al., 1972; Piper et al., 1975; Bengtsson et al., 1978a,b; Hakkarainen et al., 1978; Tiege and Nafstad, 1978; Simesen et al., 1982). In addition, vitamin E may be involved in the mastitis-metritis-agalactia (MMA) complex of sows (Ringarp, 1960; Ullrey et al., 1971; Whitehair et al., 1984).
Information is available on the vitamin E requirements for reproduction (Hanson and Hathaway, 1948; Adamstone et al., 1949; Cline et al., 1974; Malm et al., 1976; Young et al., 1977, 1978; Wilkinson et al., 1977a; Nielsen et al., 1979; Piatkowski et al., 1979; Mahan, 1991, 1994). Placental transfer of tocopherol from dam to fetus is minimal, so the offspring must rely on colostrum and milk to meet their daily needs. The content of vitamin E in sow colostrum and milk is dependent on the vitamin E content of the sow's diet (Mahan, 1991). In most studies, diets containing 5 to 7 mg/kg of vitamin E and 0.1 mg/kg of inorganic selenium have prevented deficiency lesions and supported normal reproductive performance. But the addition of 0.1 mg/kg of inorganic selenium and 22 mg/kg of vitamin E to diets appears necessary to maintain tissue vitamin E levels (Piatkowski et al., 1979). Recent research (Mahan, 1991; 1994; Wuryastuti et al., 1993), however, suggests that vitamin E levels as high as 44 to 60 mg/kg during gestation and lactation may be necessary to maximize both litter size and immunocompetency. As a result of these recent findings, the vitamin E requirements for gestation and lactation have been increased to 44 IU/kg of diet.
Vitamin E toxicity has not been demonstrated in swine. Levels as high as 550 mg/kg of diet have been fed to growing pigs without toxic effects (Bonnette et al., 1990).
Vitamin K
Although it was the last of the four fat-soluble vitamins to be discovered, the metabolic role of vitamin K has been more clearly defined than that of vitamins A, D, and E (Suttie, 1980; Kormann and Weiser, 1984). Vitamin K is essential for the synthesis of prothrombin, factor VII, factor IX, and factor X, which are necessary for the normal clotting of blood. These proteins are synthesized in the liver as inactive precursors. The action of vitamin K converts them to biologically active compounds (Suttie and Jackson, 1977; Suttie, 1980). This activation occurs by enzymatic γ-carboxylation of specific glutamate residues. The resulting carboxyglutamate residues are strong chelator of calcium ions, which are essential for blood coagulation. A deficiency of vitamin K or the presence of anticoagulation compounds reduces the number of carboxyglutamate residues, result-
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ing in a loss of activity and prolonged bleeding times. In addition to its role in blood clotting, there is evidence that vitamin K—dependent protein and peptides may be involved in calcium metabolism (Suttie, 1980; Kormann and Weiser, 1984).
Vitamin K exists in three series: the phylloquinones (K1) in plants; the menaquinones (K2), formed by microbial fermentation; and the menadiones (K3), which are synthetic. Menadione (2-methyl-1,4-naphthoquinone) is the synthetic form of vitamin K, which has the same cyclic structure as vitamins K1 and K2. All three forms of vitamin K are biologically active.
Water-soluble forms of menadione are commonly used to supplement swine diets. The major forms are menadione sodium bisulfite (MSB) and menadione dimethylpyrimidinol bisulfite (MPB). Menadione sodium bisulfite complex (MSBC) is used in poultry diets, but it does not have FDA approval for use in swine diets. The vitamin K activity depends upon the menadione content of these products: 52, 33, and 46 percent menadione in MSB, MSBC, and MPB, respectively. Menadione nicotinamide bisulfite is a new synthetic form of vitamin K that has been shown to have a bioactivity similar to that of MPB (Oduho et al., 1993).
Vitamin K deficiency increases prothrombin and clotting times and may result in internal hemorrhages and death (Schendel and Johnson, 1962; Brooks et al., 1973; Seerley et al., 1976; Hall et al., 1986, 1991). Schendel and Johnson (1962) reported a requirement of 5 µg of menadione sodium phosphate/kg of body weight for 1- and 2-day-old pigs fed a purified liquid diet. Their diet contained sulfathiazole and oxytetracycline to reduce the intestinal synthesis of vitamin K. Wire-bottomed cages were used and carefully cleaned to minimize coprophagy. Seerley et al. (1976) reported that 1.1 mg of MPB/kg of diet counteracted the effects of the anticoagulant pivalyl in weanling pigs. Hall et al. (1986) suggested that 2 mg/kg of menadione as MPB was needed to counteract the effects of pivalyl in growing pigs.
Bacterial synthesis of vitamin K and subsequent absorption, directly or by coprophagy, reduces or eliminates the need for supplemental vitamin K. High levels of antibiotics may decrease the synthesis of vitamin K by the intestinal flora. Studies have not been conducted to determine whether a supplemental source of vitamin K is beneficial for the breeding herd.
Muhrer et al. (1970), Osweiler (1970), and Fritschen et al. (1971) reported an occurrence of hemorrhagic conditions in pigs under field conditions. Mycotoxin-contaminated ingredients were suspected in these incidents, and vitamin K supplementation (2.0 mg of menadione/kg of diet) prevented the hemorrhagic syndrome. In some of these studies, the presence of anti-clotting coumarins may have increased the dietary requirement for vitamin K. Excess calcium may also increase the pig's requirement for vitamin K (Hall et al., 1991). Liver stores of vitamin K can be depleted very rapidly during even very short periods of vitamin K—deficient diet consumption (Kindberg and Suttie, 1989).
Stability of water-soluble menadione supplements in premixes and diets is impaired by moisture, choline chloride, trace elements, and alkaline conditions. Coelho (1991) suggested that MSBC and MPB can lose up to 80 percent of bioactivity if stored for 3 months in a vitamin—trace—mineral premix containing choline. Activity losses were far less when the menadione compounds were stored in the same premix that did not contain choline. Some menadione supplements are now coated, and this appears to improve stability in diets and premixes.
Even very large amounts of menadione compounds are tolerated well by animals. Seerley et al. (1976) fed 110 mg/kg of MPB to pigs, and Oduho et al. (1993) fed 300 mg/kg of MPB to chicks; neither observed signs of toxicity. A dietary level of 3,000 mg/kg of MPB did not depress weight gain or blood hemoglobin when fed over a 14-day period to chicks. It appears that menadione levels of 1,000 times an animal's requirement are well tolerated (National Research Council, 1987; Oduho et al., 1993).
Water-Soluble Vitamins
Biotin
Biotin is important metabolically as a cofactor for several enzymes that function in carbon dioxide fixation. As part of pyruvate carboxylase and propionyl CoA carboxylase, it is important in gluconeogenesis and in the citric acid cycle. Acetyl CoA carboxylase is also a biotin-dependent enzyme that functions in initiating fatty acid biosynthesis. Whitehead et al. (1980) and Misir and Blair (1986) suggested that plasma biotin concentration and plasma pyruvate carboxylase activity are methods of assessing the biotin status of pigs. The D-isomer of biotin is the biologically active form of the vitamin.
Biotin is present in most common feedstuffs in more-than-adequate amounts, but its bioavailability varies greatly among ingredients. The bioavailability of biotin in yellow corn and soybean meal is high for the chick, but its bioavailability in barley, grain sorghum, oats, and wheat is lower (Frigg, 1976; Anderson et al., 1978; Kopinski et al., 1989). Much of the biotin in feed ingredients exists as ε-N-biotinyl L-lysine (biocytin), which is a component of protein. The bioavailability of biocytin (relative to crystalline D-biotin) varies widely and is dependent on the digestibility of the proteins in which it is found. A considerable portion of the pig's biotin requirement is presumed to come from bacterial synthesis in the gut.
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In general, performance has not been improved by supplemental biotin in a wide range of diets and conditions for pigs weaned at 2 to 28 days of age or for growing-finishing pigs. Pigs from 2 to 28 days of age fed a filtered skim milk diet containing about 10 µg of biotin/kg of dry matter (about 15 percent of the level in sow's milk) gained weight and were as efficient in feed conversion as littermate pigs supplemented with 50 µg of biotin/kg of diet (New-port, 1981). Likewise, biotin supplementation at levels varying from 110 to 880 µg/kg of diet yielded no improvement in rate or efficiency of gain in pigs weaned at 21 to 28 days of age or in growing-finishing pigs (Peo et al., 1970; Hanke and Meade, 1971; Meade, 1971; Washam et al., 1975; Simmins and Brooks, 1980; Easter et al., 1983; Bryant et al., 1985b; Hamilton and Veum, 1986). Exceptions include one experiment that Adams et al. (1967) reported for growing pigs and one experiment that Peo et al. (1970) reported for pigs weaned at 28 days of age. Also, Partridge and McDonald (1990) observed feed efficiency responses to biotin when it was added to wheat—barley—soybean meal diets for growing pigs.
With sows, biotin supplementation has been reported to improve hoof hardness and compression, compressive strength, and the condition of skin and hair coat, as well as to reduce hoof cracks and footpad lesions (Grandhi and Strain, 1980; Webb et al., 1984; Bryant et al., 1985a,b; Simmins and Brooks, 1985; Misir and Blair, 1986). However, in studies by Hamilton and Veum (1984) and Tribble et al. (1984), no such improvements were recorded.
Lewis et al. (1991) reported that adding 0.33 mg/kg of biotin to a corn—soybean meal diet for sows during both gestation and lactation increased the number of pigs weaned but did not improve foot health. Watkins et al. (1991) also conducted a large-scale biotin efficacy trial for sows during gestation and lactation and reported that none of the criteria of reproductive performance, progeny development, or foot health responded to 0.44 mg of supplemental biotin/kg of diet. Other studies by investigators using a variety of grain sources have resulted in inconsistent results (Brooks et al., 1977; Penny et al., 1981; Easter et al., 1983; Simmins and Brooks, 1983; Hamilton and Veum, 1984; Tribble et al., 1984; Bryant et al., 1985c; Kornegay, 1986; Misir and Blair, 1986). A lack of consistency among experiments and a wide range of biotin supplementation levels (0.1 to 0.55 mg/kg of diet) make it difficult to establish a specific biotin requirement for sows.
Biotin deficiency signs include excessive hair loss, skin ulcerations and dermatitis, exudate around the eyes, inflammation of the mucous membranes of the mouth, transverse cracking of the hooves, and the cracking or bleeding of the footpads (Cunha et al., 1946; 1948; Lindley and Cunha, 1946; Lehrer et al., 1952). Biotin deficiency in pigs has been produced by feeding pigs synthetic diets containing sulfa drugs, which presumably reduce the synthesis of biotin in the intestinal tract (Lindley and Cunha, 1946; Cunha et al., 1948; Lehrer et al., 1952). Incorporation of large amounts of desiccated eggwhite in synthetic diets also has precipitated biotin deficiency in pigs (Cunha et al., 1946; Hamilton et al., 1983). Avidin, contained in raw eggwhite, forms a complex with biotin in the intestinal tract, rendering the vitamin unavailable to the pig.
Choline
Choline remains in the B-vitamin category even though the quantity required far exceeds the "trace organic nutrient" definition of a vitamin. It is generally added to swine diets as choline chloride, which contains 74.6 percent choline activity (Emmert et al., 1996). Choline is required for (a) phospholipid (i.e., lecithin) synthesis, (b) acetyl choline formation, and (c) transmethylation of homocysteine to methionine, which occurs via betaine, the oxidation product of choline. When severe choline deficiency is encountered, phospholipid and acetyl choline synthesis take priority over choline's methylation functions; however, grain—oilseed meal diets contain enough choline such that betaine or choline is equally efficacious on a molar basis in meeting the methylation function of choline (Lowry et al., 1987).
Pigs synthesize choline by methylating phosphatidyl ethanolamine in a three-step process involving methyl transfer from S-adenosylmethionine. Thus, excess dietary methionine can eliminate the dietary need for choline in pigs (Neumann et al., 1949; Nesheim and Johnson, 1950; Kroening and Pond, 1967).
Choline from soybean meal has been estimated to be 65 to 83 percent bioavailable relative to choline from choline chloride (Molitoris and Baker, 1976; Emmert and Baker, 1997). Analytical and bioavailability studies with chicks have indicated that dehulled soybean meal contains 2,218 mg of total choline/kg and 1,855 mg of bioavailable choline/kg; bioavailability of choline in peanut meal (71 percent) was slightly less than that in soybean meal (83 percent) and the choline in canola meal was only 24 percent bioavailable (Emmert and Baker, 1997). Because soy products are rich in bioavailable choline, starting, growing, and finishing pigs have not shown responses to supplemental choline when it was added to corn—soybean meal or corn-isolated soy protein diets (Bryant et al., 1977; Russett et al., 1979b; North Central Region-42 Committee on Swine Nutrition, 1980). A portion of the choline present in feed ingredients and unprocessed fat sources exists as phospholipid-bound choline. This form of choline is thought to be utilized well (Emmert et al., 1996), but refined oils have been subjected to degumming, and this process removes virtually all of the phospholipid-bound choline (Anderson et al., 1979).
Feeding pregnant gilts and sows grain—soybean meal diets supplemented with 434 to 880 mg of choline/kg has
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generally increased the number of live pigs born and weaned (Kornegay and Meacham, 1973; Stockland and Blaylock, 1974; North Central Region-42 Committee on Swine Nutrition, 1976; Grandhi and Strain, 1980). In a long-term reproduction study, Stockland and Blaylock (1974) also reported that choline supplementation of corn–soybean meal diets improved conception rate. Gilts fed a choline-supplemented diet during gestation farrowed heavier pigs, but the incidence of spraddle-legged pigs was not reduced in four trials reported by Luce et al. (1985). During lactation, choline supplementation of diets containing 8 to 10 percent fat or oil did not improve lactation performance (Seerley et al., 1981; Boyd et al., 1982).
Choline-deficient pigs have reduced weight gain, rough hair coats, decreased red blood cell counts and hematocrit and hemoglobin concentrations, increased plasma alkaline phosphatase, and unbalanced and staggering gaits. Livers and kidneys exhibit fat infiltration. In a severe choline deficiency, kidney glomeruli can become occluded from massive fat infiltration (Wintrobe et al., 1942; Johnson and James, 1948; Neumann et al., 1949; Russett et al., 1979b).
The addition of 260 mg of choline/kg to a diet consisting of 30 percent vitamin-free casein, 37 percent glucose, 26.6 percent lard, and 2 percent sulfathaladine, which contained 0.8 percent methionine, prevented a choline deficiency in neonatal pigs (Johnson and James, 1948). A level of 1,000 mg of choline/kg of diet solids optimized weight gain and feed efficiency and prevented fat infiltration of the liver and kidneys in 2-day-old pigs (Neumann et al., 1949). Further addition of 0.8 percent DL-methionine to this diet did not improve the performance of pair-fed pigs supplemented with 1,000 mg of choline/kg of diet (Nesheim and Johnson, 1950). Kroening and Pond (1967) fed 5-kg pigs a low-protein (12 percent) diet supplemented with three levels of DL-methionine: 0, 0.11, or 0.22 percent. The addition of 1,646 mg of choline/kg of diet tended to improve the weight gains and feed conversion of pigs fed the two lower levels of methionine but not those of pigs fed the diet containing 0.22 percent supplemental methionine. Russett et al. (1979a, b) reported a minimum choline requirement of 330 mg/kg of diet for 6- to 14-kg pigs fed a semisynthetic diet containing 0.31 percent methionine and 0.33 percent cystine.
No signs of choline toxicity have been reported in swine (National Research Council, 1987), but daily gain reductions have been observed in pigs fed diets containing 2,000 mg/kg of added choline during the starting, growing, and finishing stages (Southern et al., 1986). In another study (Emmert 1997), a dietary choline level of 10,000 mg/kg did not depress growth in 10-kg pigs, nor did a similar level of betaine.
Folacin
Folacin includes a group of compounds with folic acid activity. Chemically, folacin consists of a pteridine ring, paraaminobenzoic acid (PABA), and glutamic acid. Animal cells cannot synthesize PABA, nor can they attach glutamic acid to pteroic acid. A deficiency of folacin causes a disturbance in the metabolism of single-carbon compounds, including the synthesis of methyl groups, serine, purines, and thymine. Folacin is involved in the conversion of serine to glycine and homocysteine to methionine.
The folacin present in feedstuffs exists primarily as a polyglutamate conjugate containing a γ-linked polypeptide chain of seven glutamic acid residues. A group of intestinal enzymes known as conjugases (folyl polyglutamate hydrolases) remove all but the last glutamate residue. Only the monoglutamyl form is thought to be absorbed into the intestinal enterocyte. Most of the folacin taken up by the intestinal brush border is reduced to tetrahydrofolic acid (FH4) and then methylated to 5N-methyl FH4. Like thiamin, folacin has a free amino group (on the pteridine ring), and this makes it heat-labile, particularly in diets containing reducing sugars such as dextrose or lactose.
Except for the studies of Matte et al. (1984a,b; 1992) and Lindemann and Kornegay (1986; 1989), results have indicated that the folacin contribution of ingredients commonly fed to swine when combined with bacterial synthesis within the intestinal tract adequately meets the requirement for all classes of swine.
Supplementation of a corn–soybean meal diet with 200 µg of folic acid/kg of diet during pregnancy did not increase the number of pigs born alive or weaned (Easter et al., 1983). Matte et al. (1984a) administered 15 mg of folic acid intramuscularly to sows 10 times, beginning at weaning and continuing until day 60 of pregnancy. They reported a significant increase in litter size farrowed. In a subsequent study, Matte et al. (1992) observed an increase in litter growth rate when the gestation diet was supplemented with 5 or 15 mg/kg of folic acid. Supplementation of the lactation diet, however, did not improve performance of the offspring. Lindemann and Kornegay (1989) also observed increased litter size at birth, but not at weaning, when the corn–soybean meal diet fed to sows was supplemented with 1 mg/kg of folacin. In a study by Tremblay et al. (1986), 4.3 mg of supplemental folic acid/kg of diet (diet containing 0.62 mg of folic acid/kg) maintained serum folate concentrations equivalent to those of pregnant sows injected with folic acid at various intervals from weaning to 56 days after mating (10 injections of 15 mg/sow). In a large multiparity study involving 393 sows, addition of 1, 2, or 4 mg/kg of folic acid to standard corn–soybean meal diets during premating, gestation, and lactation had no beneficial effects on reproductive performance (Harper et al., 1994). Based on these recent studies, the folacin requirement for gestating and lactating sows was increased to 1.3 mg/kg of diet.
Folacin deficiency in pigs leads to slow weight gain, fading hair color, macrocytic or normocytic anemia, leuko-
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penia, thrombopenia, reduced hematocrit, and bone marrow hyperplasia. Synthetic diets, generally with the inclusion of 1 to 2 percent sulfa drugs or folic acid antagonists, have been fed to produce folacin deficiency in pigs (Cunha et al., 1948; Heinle et al., 1948; Cartwright et al., 1949, 1950; Johnson et al., 1950). Sulfa drugs presumably reduce bacterial synthesis of folacin in the intestinal tract. Folic acid supplementation did not affect the performance of 4-day-old pigs fed a synthetic diet that included 2 percent sulfathaladine (Johnson et al., 1948) or of 8-week-old pigs fed a synthetic diet (Cunha et al., 1947). Newcomb and Allee (1986) reported no beneficial effects from the addition of 1.1 mg of folic acid/kg to a corn–soybean meal–whey diet for pigs weaned at 17 to 27 days of age. But Lindemann and Kornegay (1986) observed an improved daily weight gain in pigs of similar age fed a corn—soybean meal diet supplemented with 0.5 mg of folic acid/kg of diet. Pigs fed corn–soybean meal diets during the starting, growing, and finishing phases gained weight and used their feed as efficiently as those supplemented with 200 or 360 µg of folic acid/kg of diet (Easter et al., 1983; Gannon and Liebholz, 1989).
Niacin
Niacin or nicotinic acid is a component of the coenzymes nicotinamide-adenine dinucleotide (NAD) and nicotin-amide-adenine dinucleotide phosphate (NADP). These coenzymes are essential for the metabolism of carbohydrates, proteins, and lipids.
Metabolic conversion of excess dietary tryptophan to niacin has complicated the determination of the niacin requirement (Luecke et al., 1948; Powick et al., 1948). Firth and Johnson (1956) estimated that each 50 mg of tryptophan in excess of the tryptophan requirement yields 1 mg of niacin. Niacin status is further complicated by its limited bioavailability in certain feed ingredients. The niacin in yellow corn, oats, wheat, and grain sorghum is in a bound form that is largely unavailable to young pigs (Kodicek et al., 1956; Luce et al., 1966, 1967; Harmon et al., 1969, 1970). The niacin in soybean meal, however, is highly available for the chick and is probably equally available for the pig (Yen et al., 1977).
Niacin activity is commercially available as either free nicotinic acid or free nicotinamide (niacinamide). Relative to nicotinic acid, nicotinamide is 124 percent bioavailable for chicks (Oduho and Baker, 1993) and 109 percent bioavailable for rats (Carter and Carpenter, 1982).
Firth and Johnson (1956) estimated the available niacin requirements for 1- to 8-kg pigs to be about 20 mg/kg for a diet with no excess tryptophan. Requirement estimates for growing pigs weighing 10 to 50 kg are 10 to 15 mg of available niacin/kg for diets containing tryptophan levels near the requirement (Braude et al., 1946; Kodicek et al., 1959; Harmon et al., 1969). Growing-finishing diets are usually fortified with niacin, but studies with 45-kg pigs fed corn–soybean meal diets have indicated no performance improvements due to niacin supplementation (Yen et al., 1978; Copelin et al., 1980). The diets used in these experiments, however, contained calculated tryptophan levels that were in excess of the requirement. There is no information on the niacin requirement of pregnant and lactating sows.
Research with chicks has demonstrated that iron deficiency impairs the efficacy of tryptophan as a niacin precursor (Oduho et al., 1994). Whether this relationship occurs in pigs is unknown. Iron is required as a cofactor for two enzymes in the pathway leading to nicotinic acid mononucleotide synthesis from tryptophan.
Niacin deficiency signs include reduced weight gain, anorexia, vomiting, dry skin, dermatitis, rough hair coat, hair loss, diarrhea, mucosal ulcerations, ulcerative gastritis, inflammation and necrosis of the cecum and colon, and normocytic anemia (Huges, 1943; Wintrobe et al., 1946; Braude et al., 1946; Powick et al., 1947a,b; Luecke et al., 1947; Cartwright et al., 1948; Burroughs et al., 1950; Kodicek et al., 1956). Blood erythrocyte NAD activity and urinary excretions of N-methyl-nicotinamide and N'-methyl-2-pyridone-5-carboxamide are reduced in niacin deficiency (Luce et al., 1966, 1967).
Pantothenic Acid
This B-vitamin consists of pantoic acid joined to β-alanine by an amide bond. As a component of coenzyme A, pantothenic acid is important in the catabolism and synthesis of two-carbon units evolved during carbohydrate and fat metabolism. Biological availability of pantothenic acid is low in barley, wheat, and sorghum but is high in corn and soybean meal (Southern and Baker, 1981). In feedstuffs, most of the pantothenic acid exists as coenzyme A, acyl CoA synthetase, and acyl carrier protein. Only the D-isomer of pantothenic acid is biologically active. Synthetic pantothenic acid is generally added to all swine diets as calcium pantothenate, a salt that is more stable than pantothenic acid. The D-form of calcium pantothenate has 92 percent activity; the racemic mixture of the calcium salt contains only 46 percent active pantothenic acid. A DL-calcium pantothenate–calcium chloride complex is also available, and it contains 32 percent activity.
The pantothenic acid requirement of 2- to 10-kg pigs fed synthetic diets was 15.0 mg/kg (Stothers et al., 1955); and for 5- to 50-kg pigs, estimates range from about 4.0 to 9.0 mg/kg of diet (Luecke et al., 1953; Barnhart et al., 1957; Sewell et al., 1962; Palm et al., 1968). Requirement estimates for pigs weighing between 20 and 90 kg have varied from 6.0 to 10.5 mg of pantothenic acid/kg of diet (Cartron et al., 1953; Pond et al., 1960; Davey and Steven-
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son, 1963; Palm et al., 1968; Meade et al., 1969; Roth-Maier and Kirchgessner, 1977).
Ullrey et al. (1955), Davey and Stevenson (1963), and Teague et al. (1970) reported poor reproductive performance in three experiments when the pantothenic acid level was below 5.9 mg/kg of diet; Bowland and Owen (1952), however, reported normal reproductive performance at this level. Ullrey et al. (1955) and Davey and Stevenson (1963) estimated the pantothenic acid requirement for optimal reproduction at 12.0 to 12.5 mg/kg of diet.
Pantothenic acid deficiency signs include slow growth, anorexia, diarrhea, dry skin, rough hair coat, alopecia, reduced immune response, and an abnormal movement of the hind legs called goose stepping (Hughes and Ittner, 1942; Wintrobe et al., 1943b; Luecke et al., 1948, 1950, 1952; Wiese et al., 1951; Stothers et al., 1955; Harmon et al., 1963). Postmortem findings in pigs with pantothenic acid deficiency include edema and necrosis of the intestinal mucosa, increased connective tissue invasion of the submucosa, loss of nerve myelin, and degeneration of dorsal root ganglion cells (Wintrobe et al., 1943b; Follis and Wintrobe, 1946).
Riboflavin
A component of two coenzymes, flavin mononucleotide (FMN) and flavin adenine dinucleotide (FAD), riboflavin is important in the metabolism of proteins, fats, and carbohydrates. In feedstuffs, most of the riboflavin activity exists as FAD.
Estimates of the riboflavin requirement for pigs weighing 2 to 20 kg range from 2.0 to 3.0 mg/kg of synthetic diet (Forbes and Haines, 1952; Miller et al., 1954). Riboflavin requirement estimates range from 1.1 to 2.9 mg/kg for growing pigs fed synthetic diets (Hughes, 1940a; Krider et al., 1949; Mitchell et al., 1950; Terrill et al., 1955), whereas the estimates vary from 1.8 to 3.1 mg/kg of diet when practical diets are fed (Krider et al., 1949; Miller and Ellis, 1951). Seymour et al. (1968) reported no consistent interactions between riboflavin level and environmental temperature for 5- to 17-kg pigs, a finding that contradicted an earlier report by Mitchell et al. (1950). Corn–soybean meal diets are deficient in bioavailable riboflavin. In a study with chicks, Chung and Baker (1990) estimated that the riboflavin in corn–soybean meal diets is 59 percent bioavailable relative to crystalline riboflavin.
Riboflavin deficiency has led to anestrus (Esch et al., 1981) and reproductive failure in gilts (Miller et al., 1953; Frank et al., 1984). On the basis of farrowing performance and erythrocyte glutathione reductase activity (FAD-dependent enzyme), Frank et al. (1984) estimated the available riboflavin requirement for pregnancy to be about 6.5 mg daily. Pettigrew et al. (1996), however, observed that 60 mg of riboflavin/day produced a higher farrowing rate than 10 mg/day when these levels were fed from breeding to day 21 of gestation. Erythrocyte glutathione reductase activity and farrowing performance suggest a lactation requirement of about 16 mg of riboflavin daily (Frank et al., 1988).
Signs of riboflavin deficiency in young growing pigs include slow growth, cataracts, stiffness of gait, seborrhea, vomiting, and alopecia (Wintrobe et al., 1944; Miller and Ellis, 1951; Lehrer and Wiese, 1952; Miller et al., 1954). In severe riboflavin deficiency, researchers have observed increased blood neutrophil granulocytes, decreased immune response, discolored liver and kidney tissue, fatty liver, collapsed follicles, degenerating ova, and degenerating myelin of the sciatic and brachial nerves (Wintrobe et al., 1944; Krider et al., 1949; Mitchell et al., 1950; Forbes and Haines, 1952; Lehrer and Wiese, 1952; Miller et al., 1954; Terrill et al., 1955; Harmon et al., 1963).
Thiamin
Thiamin is essential for carbohydrate and protein metabolism. The coenzyme, thiamin pyrophosphate, is essential for the oxidative decarboxylation of α–keto acids. Thiamin is very heat-labile. Therefore, excess heat or autoclaving can reduce the thiamin content of dietary components, particularly when reducing sugars are present.
Miller et al. (1955) estimated a thiamin requirement of 1.5 mg/kg for pigs weighing about 2 kg initially and fed to approximately 10 kg of body weight. Pigs weaned at 3 weeks and fed to about 40 kg of body weight required about 1.0 mg of thiamin/kg of diet (Van Etten et al., 1940; Ellis and Madsen, 1944). The survival time of thiamin-deficient pigs was increased by increasing fat levels to 28 percent of the diet (Ellis and Madsen, 1944). This finding indicated that the requirement for thiamin was decreased as the dietary energy from carbohydrate was replaced with higher levels of fat. Weight gain was improved by increasing thiamin levels to 1.1 mg/kg of diet, whereas feed intake was maximized at 0.85 mg/kg of diet for pigs weighing about 30 kg and fed to 90 kg of body weight (Peng and Heitman, 1974). Peng and Heitman (1973) evaluated the thiamin status of growing-finishing pigs by measuring the increase in erythrocyte transketolase activity resulting from thiamin pyrophosphate addition to in vitro preparations. This criterion yielded thiamin requirement estimates up to four times the level required for maximum weight gain. Furthermore, the requirement measured by this criterion increased as environmental temperature increased from 20 to 35°C (Peng and Heitman, 1974). This change was probably related to a reduction in feed intake. There is a lack of information on the thiamin requirement for pregnancy and lactation.
Treatment of feed ingredients with sulfur dioxide inactivates thiamin. This process was used in early studies to
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produce deficient diets for purposes of determining a pig's thiamin requirement (Van Etten et al., 1940; Ellis and Madsen, 1944). A number of freshwater fish species contain an antithiamin factor known as thiaminase I (Tanphaichitr and Wood, 1984). Feeding moderate levels of unprocessed freshwater fish preparations to other animals can cause a thiamin deficiency (Green et al., 1941; Krampitz and Woolley, 1944).
Thiamin-deficient pigs exhibit loss of appetite; a reduction in weight gain, body temperature, and heart rate; and, occasionally, vomiting. Other effects observed in thiamin deficiency are heart hypertrophy, flabby heart, myocardial degeneration, and sudden death because of heart failure. Animals deficient in thiamin also have elevated plasma pyruvate concentrations (Hughes, 1940b; Van Etten et al., 1940; Follis et al., 1943; Wintrobe et al., 1943a; Ellis and Madsen, 1944; Heinemann et al., 1946; Miller et al., 1955). Most of the cereal grains used in swine diets are rich in thiamin. Hence, grain–oilseed meal diets fed to all classes of swine are considered adequate in this B-vitamin, and it is not generally included as a supplement for swine diets.
Vitamin B6 (The Pyridoxines)
Vitamin B6 occurs in feedstuffs as pyridoxine, pyridoxal, pyridoxamine, and pyridoxal phosphate. Pyridoxal phosphate is an important cofactor for many amino acid enzyme systems, including transminases, decarboxylases, dehydratases, synthetases, and racemases. Vitamin B6 plays a crucial role in central nervous system function. It is involved in the decarboxylation of amino acid derivatives for the synthesis of neurotransmitters and neuroinhibitors.
Vitamin B6 in corn and soybean meal is about 40 and 60 percent bioavailable for the chick, respectively (Yen et al., 1976). Presumably, it is the same in pigs, although data are not available. Miller et al. (1957) and Kösters and Kirchgessner (1976a,b) suggested a dietary requirement of 1.0 to 2.0 mg/kg of diet for the pig weighing initially about 2 kg and fed to 10 kg of body weight. Requirement estimates for the 10- to 20-kg pig range from 1.2 to 1.8 mg of vitamin B6/kg of diet (Sewall et al., 1964; Kösters and Kirchgessner, 1976a,b).
Ritchie et al. (1960) reported no treatment differences in reproductive or lactation performance in gilts and sows fed diets containing total pyroxidine levels of either 1.0 or 10.0 mg/kg from the second month of pregnancy through day 35 of lactation. Easter et al. (1983) reported an increase in litter size at birth and at weaning when 1.0 ppm of pyridoxine was added to a corn–soybean meal diet fed to gilts during pregnancy. In another study, the coefficients of glutamic-oxaloacetic transaminase activity in red blood cells of sexually mature gilts fed 0.45 and 2.1 mg of vitamin B6/day were elevated compared with those of gilts fed an excess level of 83 mg of vitamin B6/day. Whole muscle glutamic-oxaloacetic transaminase activity was reduced in deficient gilts; this reduction suggests that the daily requirement for vitamin B6 may be greater than 2.1 mg (Russell et al., 1985a,b).
A deficiency of vitamin B6 will reduce appetite and growth rate. Advanced deficiency will result in an exudate development around the eyes, convulsions, ataxia, coma, and death. Blood samples from deficient pigs show a reduction in hemoglobin, red blood cells, and lymphocyte counts. Serum iron and gamma globulin are increased. Peripheral myelin and axis cylinder degeneration of the sensory neurons, microcytic hypochromic anemia, and fat infiltration of the liver are characteristic of vitamin B6 deficiency (Hughes and Squibb, 1942; Wintrobe et al., 1942, 1943c; Follis and Wintrobe, 1946; Lehrer et al., 1951; Miller et al., 1957; Harmon et al., 1963). A tryptophan-loading test, in which the conversion of tryptophan to niacin is impaired, can determine vitamin B6 status. This impairment results in elevated xanthurenic acid and kynurenic acid concentrations in the urine (Cartwright et al., 1944). Supplementation of grain–soybean meal diets with vitamin B6 is generally unnecessary, because the level of bioavailable vitamin B6 in feed ingredients will meet the pig's requirement.
Vitamin B12
Vitamin B12, or cyanocobalamin, contains the trace element cobalt in its molecule, which is a unique feature among vitamins. Vitamin B12 as a coenzyme is involved in the de novo synthesis of labile methyl groups derived from formate, glycine, or serine, and their transfer to homocysteine to form methionine. It is also important in the methylation of uracil to form thymine, which is converted to thymidine and used for the synthesis of DNA. Pigs require vitamin B12, but responses to dietary supplementation have been variable. Synthesis of vitamin B12 by microorganisms in the environment and within the intestinal tract as well as the pig's inclination toward coprophagy may supply sufficient vitamin B12 to satisfy the pig's requirement (Bauriedel et al., 1954; Hendricks et al., 1964). Ingredients of plant origin are devoid of vitamin B12, but animal and fermentation by-products contain the vitamin. In these ingredients, vitamin B12 exists in a methylated form (methylcobalamin) or a 5'-deoxyadenosyl form (adenosyl cobalamin), and both of these compounds are generally bound to protein. Vitamin B12 supplements are produced commercially by microbial fermentation and are usually added to grain–soybean meal diets.
Receptor sites for vitamin B12 binding are located in the ileum. Prior to absorption, cobalamin is bound to a glycoprotein, commonly referred to as "intrinsic factor." Intrinsic factor is derived from the parietal cells of gastric mucosa. Vitamin B12 is stored effectively in the body. Thus tissue storage, primarily in the liver, resulting from excess
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vitamin B12 ingestion can delay for many months the onset of vitamin B12 deficiency symptoms after a vitamin B12-deficient diet is fed.
Estimated vitamin B12 requirements for 1.5- to 20-kg pigs fed synthetic milk diets and housed in wire-floored cages range from 15 to 20 µg/kg of dietary dry matter (Anderson and Hogan, 1950b; Nesheim et al., 1950; Frederick and Brisson, 1961), but as high as 50 µg/kg of diet dry matter in one study (Neumann et al., 1950). Pigs weighing about 10 to 45 kg required 8.8 to 11.0 µg of vitamin B12/kg of diet (Richardson et al., 1951; Catron et al., 1952). The animals in these experiments also were housed in wire-floored cages.
Anderson and Hogan (1950a), Frederick and Brisson (1961), and Teague and Grifo (1966) improved the reproductive performance of sows by adding 11 to 1,100 µg of vitamin B12/kg of diet. Teague and Grifo (1966) compared the reproductive performance of sows fed an unsupplemented all-plant diet with that of a diet supplemented with 110 to 1,100 µg/kg of vitamin B12. Until the sows' third and fourth parities, there was no reduction in the number of pigs farrowed or weaned, or in their weights at birth or weaning. Because of the wide range of levels supplemented and the few experiments, it is difficult to determine the vitamin B12 requirement for reproduction and lactation, but it is estimated at 15 µg/kg of diet.
Pigs that are deficient in vitamin B12 display reduced weight gain, loss of appetite, rough skin and hair coat, irritability, hypersensitivity, and hind leg incoordination. Blood samples from deficient pigs indicate normocytic anemia and high neutrophil and low lymphocyte counts (Anderson and Hogan, 1950b; Neumann and Johnson, 1950; Neumann et al., 1950; Cartwright et al., 1951; Richardson et al., 1951; Catron et al., 1952). A deficiency of folic acid and vitamin B12 has led to macrocytic anemia and bone marrow hyperplasia, both of which have several similar characteristics to pernicious anemia in human beings (Johnson et al., 1950; Cartwright et al., 1952). Signs of folacin deficiency generally accompany vitamin B12 deficiency, because vitamin B12 is required for folate metabolism. Lack of either folacin or vitamin B12 prevents the proper transfer of methyl groups in the synthesis of thymidine.
Vitamin C (Ascorbic Acid)
Vitamin C (ascorbic acid) is a water-soluble antioxidant that is involved in the oxidation of aromatic amino acids, synthesis of norepinephrine and carnitine, and in the reduction of cellular ferritin iron for transport to the body fluids. Ascorbic acid is also essential for hydroxylation of proline and lysine, which are integral constituents of collagen. Collagen is essential for growth of cartilage and bone. Vitamin C enhances the formation of both bone matrix and tooth dentin. In vitamin C deficiency, petechial hemorrhages occur throughout the body. A dietary source of vitamin C is essential for primates and guinea pigs, but farm animals, including pigs, can synthesize this vitamin from D-glucose and several other related compounds (Braude et al., 1950; Dvorak, 1974; Brown and King, 1977). Strittmatter et al. (1978), Cleveland et al. (1983), and Nakano et al. (1983) have investigated the role of vitamin C in the prevention or alleviation of osteochondrosis in swine. These authors postulated that osteochondrosis might be related to insufficient collagen cross-linking because of reduced hydroxylation of lysine. Dietary supplementation with vitamin C, however, was ineffective in preventing this malady.
Under some conditions, pigs may not be able to synthesize vitamin C rapidly enough to meet their requirements. Riker et al. (1967) reported that plasma ascorbic acid concentrations were lower for pigs at an environmental temperature of 29°C than for pigs at 18°C. However, vitamin C supplementation of pigs housed at temperatures of either 19 or 27°C did not improve rate or efficiency of weight gain (Kornegay et al., 1986). Brown et al. (1970) found a significant correlation between energy intake and serum ascorbate levels, and later reported that vitamin C supplementation significantly improved the rate of weight gain of 3-week-old pigs (Brown et al., 1975). There was a greater response to vitamin C at a low-energy intake than at an intermediate- or a high-energy intake. The concentration and total amount of vitamin C in the liver of 1- or 40-day-old pigs was reduced in fasted pigs compared with that in suckling pigs (Dvorak, 1974). There also are reports of improved weight gains in response to supplemental vitamin C in the diet when no deliberate stress had been imposed on pigs. Jewell et al. (1981) reported improved weight gain from vitamin C supplementation in 1-day-old weaned pigs in one trial, but no response to the supplement in a second trial. Using pigs weaned at 3 to 4 weeks of age, Brown et al. (1975), Yen and Pond (1981), and Mahan et al. (1994) reported that weight gains were improved by supplementing the diet with vitamin C. In pigs weighing 24 kg initially, Mahan et al. (1966) observed an improvement in weight gain from parenteral dosing and feed supplementation with vitamin C. In two of three trials, growing pigs (15 to 27 kg) fed to about 90 kg of body weight responded to vitamin C supplementation (Cromwell et al., 1970). Others have noted no improvement in performance from vitamin C supplementation in suckling pigs, pigs weaned at 3 to 4 weeks of age, or growing-finishing pigs (Hutagalung et al., 1969; Leibbrandt, 1977; Strittmatter et al., 1978; Mahan and Saif, 1983; Nakano et al., 1983; Yen and Pond, 1984; Yen et al., 1985; Kornegay et al., 1986). Mahan et al. (1994) observed no beneficial effects from adding ascorbate to corn–soybean meal diets fed to growing-finishing pigs. Chiang et al. (1985) reviewed the effects of supplemental vitamin C for weanling and growing-finishing pigs.
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Sandholm et al. (1979) reported a rapid cessation of navel bleeding in newborn pigs when 1.0 g of vitamin C/day was fed to pregnant sows beginning 5 days before expected farrowing. Pigs from sows given supplemental ascorbic acid were significantly heavier at 3 weeks of age than those from control sows. A water-soluble vitamin K administered in the drinking water to several sows in this herd failed to prevent the navel bleeding problem in newborn pigs. In subsequent studies, there was no improvement in pig survival or growth rate when sows were supplemented with 1.0 to 10.0 g of ascorbic acid/day beginning in late pregnancy (Lynch and O'Grady, 1981; Chavez, 1983; Yen and Pond, 1983). Navel bleeding was not considered to be a problem in these latter experiments.
Currently, the conditions in which supplemental vitamin C may be beneficial are not well defined. Therefore, no vitamin C requirement estimate is given for pigs.
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Representative terms from entire chapter:
pigs fed
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