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The dietary biotin requirement (NRC, 1998) for breeding swine is estimated to be 0.2 mg per kg (0.09 mg per lb) and for growing pigs, 0.05 to 0.08 mg per kg (0.02 to 0.04 mg per lb). Requirements for biotin are difficult to establish due to biotin variability in feed content and bioavailability. Likewise, it is difficult to obtain a quantitative requirement for biotin, as the vitamin is synthesized by many microorganisms and certain fungi. These microorganisms are found in the lower part of the intestinal tract, a region in which absorption of nutrients is generally reduced. There is evidence in the pig, however, that intestinal microflora make a significant contribution to the body pool of available biotin (Barth et al., 1986). Kopinski et al. (1989a) reported that this microbially synthesized biotin is of little benefit to the pig, however. What is not known for the various species is the extent of microbial synthesis or the biotin availability to the host.
It has also been reported that microorganisms contribute to animal and human requirements, as the use of some sulfa drugs, such as sulfathalidine, can induce deficiency under some circumstances. Rate and extent of biotin synthesis may depend on the level of other dietary components. It has been shown that in rats and poultry, polyunsaturated fatty acids (PUFAs), ascorbic acid and other B vitamins may influence the demand for biotin. Addition of PUFAs to fat-free, biotin-deficient diets increased severity of dermal lesions (Roland and Edwards, 1971). Biotin is rapidly destroyed as feeds become rancid. Pure biotin was inactivated to an extent of 96% in 12 hours when linoleic acid of a high peroxide number was added to the diet (Pavcek and Shull, 1942). In the presence of alpha-tocopherol, this destruction amounted to only 40% after 48 hours.
Recently, Bonomi et al. (1996) conducted an experiment with biotin, which was microencapsulated by a fatty acids film and then fed to swine. These authors recommended the addition of between 200 and 400 ppb for growing swine to improve weight gain, feed utilization, killing percentage, yield of ham, meat digestibility, and meat tenderness.
Newport (1981) concluded that until they reached at least 28 days of age, 10 mg of biotin per kg dry matter was likely to be adequate for pigs weaned at 2 days of age and provided a milk substitute until 28 days of age. Peo et al. (1970) investigated the effect of protein source and antibiotic on response to biotin supplementation in baby pig diets and found no significant effects due to biotin supplementation at a level of 440 or 880 mg per kg. Washam et al. (1975) found no benefit of including 165 mg biotin per kg in a pelleted corn-based 18% protein starter swine ration. Average daily gain and feed:gain were not improved by the addition of biotin. Adams et al. (1967) reported a 7.5% increase in weight gain and 5% improvement in feed efficiency when 6.8 kg (15 lbs) specific pathogen- free (SPF) pigs were fed a corn-milo-soybean diet supplemented with biotin at 110 mg per kg (50 mg per lb) diet.
Partridge and McDonald (1990) studied the effects of supplemental biotin at the rate of 500 mg per kg diet when fed to pigs weighing 15 to 88 kg. They reported that feed:gain ratio was improved during the grower phase. There was also a tendency for improvements in feed:gain ratio in the starter and finisher phases and in carcass grading. Although it is recognized that biotin is essential for growing pigs, nutritionists have generally assumed that intestinal bacterial synthesis and basal diet ingredients adequately meet this need (Kornegay, 1986, Kopinski et al., 1989c, d). A review of the literature examining the benefits of supplemental biotin to the growing pig is summarized in Table 1. Of the data available, several investigators have reported significant improvements in rate of gain and (or) feed conversion. However, in a majority of the studies there is only a trend for improvement in feed conversion. The addition of biotin (55 to 880 mg per kg; 25 to 400 mg per lb) of diet appeared to improve feed conversion numerically regardless of the type of diet used, indicating that most practical diets are marginal in available biotin and not adequate to allow for optimal performance. Variation in responses to biotin supplementation for growing performance in pigs may depend on certain factors, such as age and dietary components, including high levels of copper supplementation and the PUFA content of the diet (Menten et al., 1987; Scherf, 1988; Kornegay et al., 1989). Results of Hamilton and Veum (1986) suggested that biotin supplementation of corn-soybean meal diets did not improve the performance of growing pigs because the basal diet provided adequate biotin levels (0.17 to 0.22 ppm). Partridge and McDonald (1990) suggested that the financial savings would greatly exceed the cost of providing biotin at a concentration of 100 mg/kg because of the likely improvement in feed:gain ratio.
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Kornegay et al. (1990) summarized field trial and university research on the effects of biotin supplementation on sow and gilt reproductive performance from 1977 to 1989 (Table 2). Reported supplemental biotin levels ranged from 100 to 550 mg per kg (45.5 to 250 mg per lb) of diet, with basal diets containing a wide variety of feedstuffs of varying composition and with total biotin levels ranging from 90 to 170 mg per kg (40.9 to 77.3 mg per lb) of diet. Many of these studies have shown beneficial effects of biotin supplementation on sow reproductive performance, including litter size, conception rate and interval from weaning to first estrus. The reduction in the interval from weaning to first estrus seems to be more responsive to supplemental biotin when delayed return to estrus was observed in control animals.
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Although improvements in sow reproductive performance have been reported in several single-parity studies, research involving four and five parities indicated that improvements in litter size were most obvious in parities subsequent to the first. Luce et al. (1995) indicated that biotin supplementation was not efficacious when included in wheat-soybean meal diets for bred gilts. The calculated value of the basal diet was 0.6 mg biotin per lb, which was lower than the recommended 0.9 mg per lb for bred gilts and sows (NRC, 1998). When 400 mg of biotin per ton of feed was supplied along with the basal diet, no differences in various indices of reproductive performance were observed due to supplementation. Penny et al. (1981) reported that the effect of biotin supplementation on sow reproduction depended on parity. For a 12 month- period, gilts and sows were assigned to the control group or the biotin supplementation group, which received 1,160 mg of biotin per day during pregnancy and 2,320 mg of biotin per day during lactation. Biotin had no effect in first-parity gilts. In the second and fourth parities, there were significant improvements due to biotin supplementation for the number of live pigs born. For some unapparent explanation, although significance was approached in the third parity, the effect was only a tendency. There was no effect from the fifth parity onward. Penny et al. (1981) concluded that biotin supplementation can increase the number of live pigs born in second and subsequent litters. Biotin may increase uterine space and placental development during mid-pregnancy (Scherf and Scott, 1989). Simmins (1985) reported the same number of corpora lutea, heavier ovaries and an increase in the length of the uterine horn of biotin-supplemented gilts compared with unsupplemented controls. Uterine horn length is a significant factor in determining the final volume of the uterus. Biotin additionally may act through prostaglandins, which are involved in the stretching phase of uterine enlargement via its role in carboxylation reactions involving PUFA synthesis (Scherf and Scott, 1989).
Foot and toe lesions, which often develop into severe problems in breeding herds maintained in confinement, may be associated with lameness and consequent culling (Penny et al., 1963; Smith and Robertson, 1971; Fritschen, 1979). It has been well established that experimentally induced biotin deficiency in young pigs (Cunha et al., 1946; Glattli et al., 1975; Kopinski et al., 1989c, d) and sows (Misir and Blair, 1986a) causes cracks in the sole and hoof that are responsive to biotin supplementation.
Numerous investigators (Brooks et al., 1977; Comben, 1978; Halama, 1979; Pedersen and Udesen, 1980; Penny et al., 1980; Brooks and Simmins, 1981; Brulisauer and Triebel, 1983; Bryant and Kornegay, 1984; Bryant et al., 1985a, c; Simmins and Brooks, 1988; Kornegay et al., 1990) have suggested that foot lesions in developing gilts and reproducing sows housed in confinement can be reduced, although not prevented, by adding biotin to diets containing commonly used feedstuffs; others (Grandhi and Strain, 1980; Hamilton and Veum, 1984; Lewis et al., 1991; Watkins et al., 1991) have reported no change in the incidence of foot lesions with biotin supplementation. Biotin supplementation was more beneficial in preventing foot lesions than in curing established foot lesions (Penny et al., 1980). Bryant et al. (1985c) indicated that the reduction in the number and frequency of foot lesions resulting from supplemental biotin was greater as the prevalence of foot lesions increased in the swine herd.
Brooks (1982) speculated that the variation of response to biotin supplementation may be due in part to the fact that clinical signs associated with biotin deficiency may resemble conditions having an alternative etiology and that response depends on the opportunities for resolution of the lesions (i.e., pigs housed on poorly designed floors have little opportunity for recovery, as continuous traumatic injury exceeds the capacity of the hoof for growth and repair).
Simmins and Brooks (1980, 1985) investigated the effect of dietary biotin on physical characteristics of pig hoof tissue using a puncture and compression strength test and examined specific regions of the hoof horn and claw. It has been reported that biotin increases the compressive strength and hardness of the hoof wall and decreases the hardness of heel bulb tissue (Brooks and Simmins, 1981; Webb et al., 1984), although the mode of action of biotin in the maintenance of hoof integrity is unclear.
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