Higher animals, including mammals, can synthesize carnitine. However, recent studies have indicated that the biosynthesis of carnitine may be limited or inadequate in certain animals. The liver and kidney of mammals are able to synthesize carnitine from lysine and methionine; however, endogenous biosynthesis alone is not sufficient to keep carnitine concentrations at adequate levels (Duran et al., 1990).
Although synthesis of carnitine in swine has not been investigated directly, when neonatal pigs are reared on formulas depleted of carnitine, plasma and tissue levels of carnitine are reduced (Baltzell et al., 1987). In comparison to adults, human neonates are either less able to synthesize carnitine or have lower stores of carnitine (Borum, 1991). Carnitine has been shown to be low in the tissues and blood of newborn piglets (Kerner et al., 1984). Furthermore, piglets that are fed a carnitine-free formula have reduced concentrations of carnitine in tissues than piglets that are allowed to nurse the sow (Borum and Sullivan, 1988).
Kerner et al. (1984) reported that while the concentrations of carnitine in newborn piglet liver and blood are low, high concentrations of carnitine are found in colostrum and milk. These authors also determined that most of the carnitine present in sow's colostrum is short-chain acylcarnitine and that half of the acylcarnitine in the sow's colostrum is isovalerylcarnitine. The large amounts of carnitine in colostrum and milk are probably responsible for the increased amounts of carnitine in the blood and liver of two-day-old piglets compared to the amounts found in newborn piglets.
Since muscle tissue is heavily dependent upon fat for energy, skeletal muscle contains as much as 90% of the total carnitine in the body (Odle, 1996). In fetal pigs, Baltzell et al. (1987) reported that both skeletal and cardiac muscle had higher concentrations of carnitine than did liver, intestine or kidney tissues and that levels in muscle continued to increase throughout gestation while the carnitine levels in the other tissues declined.
Because of the low levels of carnitine in newborn pigs, researchers have speculated that the deficiency may be tied to suboptimal utilization of fatty acids. Garber and Froseth (1984) investigated the effect of intravenous carnitine administration on the oxidation of palmitic acid in fasted neonatal pigs. The authors indicated that low animal numbers and high biological variation in their experiment did not allow them to draw definite conclusions with regard to the effects of carnitine. Although significant effects of carnitine were not evident, their data showed consistent trends for increased palmitic acid oxidation and decreased free fatty acids in serum of the carnitine-treated group.
Coffey et al. (1991) compared carnitine status and fatty acid metabolism in a variety of tissues obtained from piglets nursed by sows or fed formulas that contained high or low levels of carnitine. These investigators reported that piglets assigned to the low carnitine formula had reduced carnitine in their plasma and livers. Although oxidation of palmitate in vitro by the liver was reduced on day 7, by day 14 carnitine level did not affect liver lipid oxidation. Furthermore, glucose status, plasma lipids or ketones, and oxidation of palmitate by the longissimus muscle were not affected by level of dietary carnitine.
Honeyfield and Froseth (1991) evaluated whether carnitine limited substrate utilization in tissues of piglets from sows fed two levels of lysine or dietary fat. They concluded that carnitine did not appear to be the limiting factor for the oxidation of palmitoyl-CoA or the limiting factor of piglet energy metabolism.
Van Kempen and Odle (1993) found that L-carnitine supplementation stimulated medium-chain fatty acid (octanoate) oxidation when intravenously infused to colostrum-deprived newborn piglets. In a subsequent report (Van Kempen and Odle, 1995), the authors suggested that the effect of carnitine on oxidation of octanoate might involve facilitating the export of excess acetyl groups from muscle or increasing the uptake of octanoate into liver mitochondria.
Frank et al. (1999) evaluated the effects of two different sources of carnitine on nitrogen and energy metabolism in growing pigs. Both sources of supplemental L-carnitine were absorbed with equal efficacy, but neither affected energy or nitrogen metabolism.
In a report by Galvez et al. (1996), dietary L-carnitine was proposed to be conditionally required in situations involving young or stressed animals, animals with a potential for high productivity and animals fed high-fat diets proportionally high in plant oils. To investigate possible benefits of L-carnitine in these situations, L-carnitine was added to a conventional feed in one experiment and to an energy-rich, non-saturated fat-rich feed in a separate experiment. The effects of performance of weaning piglets with high growth potential were evaluated. Although not statistically significant, growth performance tended to be enhanced in piglets receiving 25 or 50 mg of L-carnitine per kg of diet. Feed conversion ratio was improved by L-carnitine supplementation at 50 mg per kg. A positive effect of L-carnitine supplementation on feed conversion ratio has also been reported by Jost and Bracher-Jakob (1996). However, Williamson et al. (1996) indicated that L-carnitine supplementation (50 ppm) did not affect average daily gain or feed efficiency of finishing pigs. Similarly, Johnston et al. (1999) were unable to detect an effect of carnitine on growth performance of growing pigs.
Whether carnitine supplementation might alter carcass characteristics in swine has also been the subject of investigation. Although no effect on growth performance was observed in their experiment, Owen et al. (1992) determined that carnitine supplementation during the growing-finishing phase increased loineye area. In a separate experiment (Owen et al., 1996), dietary carnitine was found to reduce fat deposition in favor of protein deposition. Furthermore, carnitine was found to positively influence amino acid metabolism and to stimulate fatty acid oxidation. However, Williamson et al. (1996) indicated that the addition of 50 ppm of L-carnitine to the diet of finishing pigs did not increase carcass leanness. Carnitine-supplemented pigs had higher tenth-rib and last-rib backfat thickness. Waylan et al. (1999) indicated that dietary L-carnitine supplementation (50 ppm) to diets of growing and finishing swine did not affect bacon characteristics. Sardi et al. (1996) explored the influence of L-carnitine on growing-fattening and slaughtering performance of Italian heavy pigs. In their report, L-carnitine was reported to tend to increase the fat content of the carcass, to significantly lower the lightness of loin and to slightly reduce ham weight loss during the seasoning period. These authors also indicated the dietary L-carnitine also slightly improved daily weight gain and feed efficiency.
Other authors have investigated the influence of dietary L-carnitine supplementation to gilts on ovulation and fertilization rate. Samland et al. (1998) determined that L-carnitine (200 ppm) addition increased ovulation rate and decreased fertilization rate of the embryos recovered. Sower et al. (1998) evaluated the effects of supplemental dietary carnitine (100 ppm) on various indices of performance and metabolism in lactating sows fed low-energy diets. Carnitine-supplemented sows produced less milk and had slower growing litters. No statistically significant differences were observed for feed intake, sow backfat, composition of milk or colostrum, muscle protein degradation, sows' concentrations of glucose, nonessential fatty acids (NEFA), glycerol, insulin, and IGF-1 in plasma or carnitine content of liver and mammary tissue samples. However, the authors indicated that carnitine content of tissue, colostrum and milk tended to be higher and that trends for metabolic indices were consistent with a reduction in body protein mobilization and with a stimulation of fatty acid oxidation in the carnitine-supplemented sows. Sower et al. (1998) concluded that under considerably catabolic conditions, supplemental dietary carnitine can influence the lactating sow's metabolism. Musser et al. (1997a) investigated the effects of L-carnitine addition (50 ppm) during lactation to diets of first-parity gilts. Although gilts supplemented with L-carnitine had lower average daily feed intake during the first week of lactation, during the second week and subsequent weeks, the average daily feed intake was not affected. No improvements in sow or litter performance were noted following the addition of L-carnitine. Likewise, in a report that included sows of differing parities, Musser et al. (1999a) were unable to observe improvements in the number of pigs or litter weights at weaning when sows were supplemented with 50, 100 or 200 ppm L-carnitine during lactation. Little effect of L-carnitine on sow and litter performance was evident. However, during gestation, Musser et al. (1997b; 1999b) determined that supplying dietary L-carnitine to the diets of sows increased litter birth and weaning weights. Furthermore, sows fed L-carnitine during gestation were heavier at weaning than were control sows. Carnitine supplementation during gestation also increased the rate of gain of last-rib fat depth. Concentrations of insulin on days 10 and 60 of gestation in sows fed L-carnitine were increased in comparison to control sows. Also, on days 60 and 90 of gestation, concentrations of IGF-1 were increased in the carnitine-supplemented sows. In the study by Musser et al. (1999b), the multiparous sows received L-carnitine at 100 mg per day during gestation and (or) 50 ppm during lactation. In agreement with their other studies utilizing lactating sows, few differences were observed by feeding 50 ppm of L-carnitine during lactation. However, compared to the control diet, supplementation of L-carnitine in either gestation, lactation or both increased the number of pigs born alive but not the total born (Musser et al., 1999b).
