In order to investigate the effects of benzoic acid on growth performance, nutrient digestibility, nitrogen balance and gastrointestinal microflora of piglets, we conducted a performance experiment and a separate balance study. The performance experiment involved four different dietary treatments: (1) basal diet (negative control); (2) basal diet supplemented with benzoic acid at 5 g/kg; (3) basal diet supplemented with benzoic acid at 10 g/kg; (4) basal diet supplemented with potassium diformate at 12 g/kg. Each dietary treatment was assigned to nine replicate groups, each consisting of two piglets. Live weight, daily weight gain, feed intake and feed conversion ratio were monitored as performance parameters over a 35-day period. Supplementation of the diet with benzoic acid resulted in a dose-dependent increase in feed intake and body weight gain and an improved feed conversion ratio. Piglets fed the diet supplemented with benzoic acid at 10 g/kg outperformed the control piglets in mean feed intake, body weight gain and feed conversion ratio by 9%, 15% and 6% respectively. Growth performance of the piglets fed the diet with benzoic acid at 10 g/kg was similar to that of piglets fed the diet supplemented with potassium diformate. In the balance experiment three groups of six piglets each were fed either a control diet or diets supplemented with benzoic acid at 5 or 10 g/kg respectively. Benzoic acid did not significantly affect nutrient digestibility but increased nitrogen retention. Piglets fed the diets supplemented with benzoic acid at 5 or 10 g/kg retained 5% and 6% more nitrogen, respectively, than control piglets. Supplementation of benzoic acid did not influence the pH value or the concentration of ammonia in the gastrointestinal tract but reduced the number of bacteria in the digesta. In the stomach the number of total aerobic, total anaerobic, lactic acid forming and gram-negative bacteria was reduced; in the duodenum the presence of benzoic acid reduced the number of gram-negative bacteria and in the ileum the number of total aerobic bacteria in a dose-dependent manner. Benzoic acid also considerably reduced the concentration of acetic acid in the duodenum. In conclusion, the data of this study suggest that benzoic acid exerts strong antimicrobial effects in the gastrointestinal tract of piglets and therefore enhances growth performance and nitrogen retention.

Recent studies showed that piglets of sows fed diets supplemented with L-carnitine grow faster during the suckling period than piglets of control sows fed diets without L-carnitine. This study was undertaken to investigate the effect of L-carnitine supplementation in sows on milk production and milk constituents. An experiment was performed in which two groups of 20 gilts each were fed diets with or without supplemental L-carnitine during pregnancy (0 vs. 125 mg L-carnitine daily/sow) and lactation (0 vs. 250 mg L-carnitine daily/sow). The experiment was continued over two reproductive cycles. L-carnitine-treated sows had larger litters (P<0.01) and higher litter weights (P<0.05) than control sows. Piglets of L-carnitine-treated sows had lower birth weights (P<0.05) but grew faster during the suckling period (P<0.01) and were heavier (P<0.05) at weaning than piglets of control sows. L-carnitine-treated sows had higher milk yields on d 11 and 18 of lactation than control sows (P<0.05). Milk of L-carnitine-treated sows had higher concentrations of total and free carnitine than milk of control sows (P<0.001); concentrations of fat, protein and lactose and the amounts of gross energy in the milk did not differ between the two groups of sows. The amounts of protein (P<0.05) and lactose (P<0.05) were higher in L-carnitine-treated sows than in control sows; the amount of energy secreted with the milk tended to be higher in carnitine-treated sows than in control sows (P<0.10). The study suggests that piglets of carnitine-treated sows grow faster during the suckling period than those of control sows because they ingest more nutrients and energy with the milk.

The effect of L-carnitine supplementation during pregnancy and lactation on performance parameters of sows was studied. The trial comprised a total of 127 sows (40 gilts, 87 mature sows) which were divided into a control and a treatment group. All animals were fed individually and received basic feed mixtures for pregnancy and lactation with low carnitine concentrations (gestation diet: 4.7 mg/kg feed, lactation diet: 12.5 mg/kg feed). The rations of the sows in the treated group were supplemented with 125 mg L-carnitine per head and day during pregnancy and 250 mg L-carnitine per head and day during lactation. The animals of the control group received identical feed mixtures in identical amounts, but without the L-carnitine supplement. L-carnitine supplementation resulted in higher sow liveweight gains between day 1 and day 85 of pregnancy. The number of piglets per litter and the number born alive did not differ between the control sows and those treated with L-carnitine. However, the L-carnitine-supplemented sows produced only half as many non-viable piglets as the control animals. Moreover, litter weight and mean birth weight of piglets from L-carnitine-treated sows were higher than in the control sows. This effect was more marked in gilts (+8% higher litter weight, +9% higher piglet weight) than in sows (+7% and +6%, respectively). Piglets from sows whose ration was supplemented with L-carnitine showed higher liveweight gains during the suckling period (+12% for gilts, +4% for sows), which is why litter weights post weaning were also higher among the sows treated with L-carnitine than in the control sows (+14% for gilts, +10% for sows). Overall, the study shows that dietary supplementation with L-carnitine during pregnancy and lactation improves the reproductive performance of sows.

Supplementation of carnitine has been shown to improve performance characteristics such as protein accretion in growing pigs. The molecular mechanisms underlying this phenomenon are largely unknown. Based on recent results from DNA microchip analysis, we hypothesized that carnitine supplementation leads to a downregulation of genes of the ubiquitin proteasome system (UPS). The UPS is the most important system for protein breakdown in tissues, which in turn could be an explanation for increased protein accretion. To test this hypothesis, we fed sixteen male, four-week-old piglets either a control diet or the same diet supplemented with carnitine and determined the expression of several genes involved in the UPS in the liver and skeletal muscle. To further determine whether the effects of carnitine on the expression of genes of the UPS are mediated directly or indirectly, we also investigated the effect of carnitine on the expression of genes of the UPS in cultured C2C12 myotubes and HepG2 liver cells. In the liver of piglets fed the carnitine-supplemented diet, the relative mRNA levels of atrogin-1, E214k and Psma1 were lower than in those of the control piglets (P < 0.05). In skeletal muscle, the relative mRNA levels of atrogin-1, MuRF1, E214k, Psma1 and ubiquitin were lower in piglets fed the carnitine-supplemented diet than that in control piglets (P < 0.05). Incubating C2C12 myotubes and HepG2 liver cells with increasing concentrations of carnitine had no effect on basal and/or hydrocortisone-stimulated mRNA levels of genes of the UPS. In conclusion, this study shows that dietary carnitine decreases the transcript levels of several genes involved in the UPS in skeletal muscle and liver of piglets, whereas carnitine has no effect on the transcript levels of these genes in cultivated HepG2 liver cells and C2C12 myotubes. These data suggest that the inhibitory effect of carnitine on the expression of genes of the UPS is mediated indirectly, probably via modulating the release of inhibitors of the UPS such as IGF-1. The inhibitory effect of carnitine on the expression of genes of the UPS might explain, at least partially, the increased protein accretion in piglets supplemented with carnitine.

This study investigated the hypothesis that dietary fats rich in lauric (C12) and myristic acid (C14) increase broiler performance and that the underlying mechanism involves antimicrobial effects on gut bacteria and changes in gut morphology. One hundred eighty 1-day-old Cobb-500 broilers were allotted to 3 groups. All groups received a basal diet consisting of maize, wheat, soybean meal, and a fat source (4.5, 7.0, 7.6, and 8.0% of fat product in the diet during d 1 to 9, 10 to 17, 18 to 27, and 28 to 35, respectively) until 35 d of age. The diet of the control group contained a fat with 67% of oleic and linoleic acid and 1.4% of C12 and C14 of total fatty acids, that of the esterified lauric and myristic acid (ELA) group a fat with 33% of esterified C12 and C14 and that of the free lauric and myristic acid (FLA) group a fat with 31% of both esterified and free (1:1) C12 and C14 (6 replicates/treatment, 10 birds/replicate). Gain and feed consumption did not differ between groups, but feed:gain was lower in FLA group as compared to the control group (P < 0.05). Carcass weight, liver weight, triglyceride content of liver and muscle, and muscle cholesterol were similar between groups; however, breast muscle weight was higher in the FLA than in the control group (P < 0.05). The villus height:crypt depth ratio of the duodenal wall did not differ between groups, but in the jejunum, it was lower in the FLA group as compared to the control group (P < 0.05). DNA copy numbers of Lactobacillus, Bifidobacteria, Enterobacteria, Escherichia coli, and Campylobacter jejuni in jejunal digesta were similar among groups. The study shows that dietary fats rich in free C12 and C14 improved feed:gain and breast muscle yield, but the observed effects could not be conclusively explained based on the parameters measured. The decreased jejunal villi:crypt ratio may point to changes in gut protein or cell turnover.