Growing pigs (n = 25; 17.8 +/- 0.1 kg) were used to study the effects of L-carnitine and protein intake on nitrogen (N) balance and body composition. Fat-supplemented (40 g soy oil/kg diet), corn-soybean meal basal diets containing low or high protein (136 or 180 g/diet) were formulated so that protein accretion would be limited by metabolizable energy (ME). Each basal diet was supplemented with 0 or 500 mg/kg L-carnitine and fed to pigs for 10 d in a nutrient balance trial. Final body composition was compared with weight and age-matched pigs measured on d 0 to calculate nutrient accretion rates. High protein feeding increased (P < 0.01) average daily gain (ADG) by 34%, as well as nitrogen digestibility (4.4%), retention (5.2%), urinary excretion (29%) and crude protein (CP) accretion (33%). Total-body carnitine accretion rate was 4.5 fold greater and total body carnitine concentration was almost 100% greater than in unsupplemented controls (P < 0.01). Irrespective of protein level, carnitine increased ADG (by 7.3%, P < 0.10) and CP accretion rate (9%, P < 0.10). Congruently, carnitine supplementation improved the efficiency of nitrogen retention (P < 0. 05) and reduced urinary nitrogen excretion (14%, P < 0.10). Carcass fat content also was reduced in carnitine-supplemented pigs (P < 0. 10). Collectively, these data support the hypothesis that carnitine can improve the efficiency of nitrogen utilization in 20-kg pigs fed energy-limited, fat-containing diets. We conclude that endogenous carnitine biosynthesis may be adequate to maintain sufficient tissue levels during growth, but that supplemental dietary carnitine (at 500 mg/kg) may be retained sufficiently so as to alter nutrient partitioning and thus body composition of 20-kg pigs.

Piglets (n = 240, 11.0+/-0.1 d old, 3.93+/-0.05 kg) were allotted to one of four treatments in a 2 x 2 factorial arrangement to examine the effects of diet physical form and nursery environment during the first 14 d after weaning on growth to market weight. During the treatment period, pigs were housed (10 pigs/ pen) in either a conventional hot nursery (30 degrees C) or a segregated-temperature nursery (cool ambient temp. of 24 degrees C, with enclosed hot-box hovers at 32 degrees C). Pigs in each environment were fed nutritionally identical diets in either liquid or dry-pellet form for 14 d. Subsequently, all pigs were fed identical dry diets and were housed in common grower-finisher facilities (penned by sex, five pigs/pen). At the end of the treatment period (d 14), pigs fed the liquid diet were 21% heavier than pigs fed the dry pellet diet (9.22 vs 7.60 kg; P < 0.001). Similarly, gain, feed intake, and gain/feed of liquid-fed pigs were 44%, 18%, and 22% greater, respectively, than observed for pigs fed the dry pellet diet. No main effect of environment was observed (P > 0.10); however, an interaction with diet physical form occurred during the early-nursery period (P < 0.01). Pigs fed the liquid diet showed better performance in the conventional nursery, whereas pigs fed the dry pellet diet were favored in the segregated-temperature nursery. No major differences in growth performance or in ultrasound carcass measurements were detected during the growing-finishing period; however, the advantage in body weight of liquid-fed pigs gained during the first 2 wk postweaning was maintained to the end of the trial (113.9 vs 110.6 kg; P < 0.05). Pigs that were fed the early-nursery diet in liquid form reached market weight (110 kg) 3.7 d sooner than the dry-fed controls (P < 0.01). Estimates of lean gain (calculated from live ultrasound data) were unaffected, suggesting that composition of growth was not altered. Collectively, these results show that liquid feeding during early life can markedly accelerate piglet growth performance and that the growth advantage is maintained to market weight, with no evidence of compensatory gain in the dry-fed control pigs.

To examine the kinetics of carnitine palmitoyltransferase-I (CPT-I) and the influence of dietary variables, young pigs (18 kg, n = 20) were fed corn-soybean meal diets supplemented with 40 g soy oil/kg and containing either 136 or 180 g crude protein/kg and either 0 or 500 mg/kg L-carnitine (2 x 2 factorial design). Diets were offered for 10 d (85% of ad libitum); CPT-I activities in liver and skeletal muscle mitochondria were determined, and enzyme kinetic constants (V:(max) and K:(m) for carnitine) were estimated. Kinetics of CPT-I in muscle were not affected by diet (P: > 0.1; carnitine K:(m) = 480 +/- 44 micromol/L). In contrast, the K:(m) for carnitine in liver was increased from 164 to 216 +/- 20 micromol/L by dietary L-carnitine supplementation (P: < 0.01) and from 169 to 211 +/- 20 micromol/L by high protein feeding (P: < 0.05). Dietary L-carnitine increased muscle and liver free carnitine concentrations by 72 and 158% over control concentrations (770 and 80 micro;mol/kg wet muscle and liver, respectively). Because tissue carnitine concentrations were within the range of the respective K:(m) for both liver and muscle tissue, it is inferred that alteration of tissue carnitine concentrations via dietary supplementation could modulate CPT-I activity in young pigs.

The effect of L-carnitine on in vivo fatty acid utilization was determined using colostrum-deprived newborn piglets fed emulsified triglycerides (TG) composed of [1-14C]octanoate (tri-8:0) or [1-14C]octadecanoate (tri-18:1). A soy protein-based liquid diet devoid of L-carnitine was fed piglets for 1 d to allow development of fatty acid-metabolizing enzymes and intestinal fat digestion and absorption before assessment of in vivo fat utilization. The radiolabeled TG were fed in isoenergetic amounts (97.7 kJ/kg(0.75)), with or without L-carnitine (1 mmol/kg(0.75)) as 30% (v/v) emulsions, using polyoxyethylene sorbitan monooleate as an emulsifier. Expired CO(2) was quantified and specific radioactivity (Bq/micromol) was determined at 20-min intervals over 24 h. The rate (mmol ATP.kg(-0.75).min(-1)) and extent (mol ATP/kg(0.75)) of TG oxidative utilization (i.e., composite of digestion, absorption and oxidation) were calculated from the kinetics of 14CO(2) expiration. The maximal rate and extent of tri-8:0 oxidation were three and fourfold greater than those of tri-18:1, respectively (P < 0.001), and tri-18:1 delayed the time to reach 10 and 50% of maximal oxidation rate by 1.2 and 1.9 h (P < 0.01, respectively), regardless of supplemental carnitine. Collectively, these findings quantify the accelerated oxidation of medium-chain vs. long-chain triglycerides, but fail to support a need for supplemental carnitine to maximize fat oxidation in colostrum-deprived piglets.

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