An 8-wk study of the effects of CLA, rendered animal fats, and ractopamine, and their interactive effects on growth, fatty acid composition, and carcass quality of genetically lean pigs was conducted. Gilts (n = 228; initial BW of 59.1 kg) were assigned to a 2 x 2 x 3 factorial arrangement consisting of CLA, ractopamine, and fat treatments. The CLA treatment consisted of 1% CLA oil (CLA-60) or 1% soybean oil. Ractopamine levels were either 0 or 10 ppm. Fat treatments consisted of 0% added fat, 5% choice white grease (CWG), or 5% beef tallow (BT). The CLA and fat treatments were initiated at 59.1 kg of BW, 4 wk before the ractopamine treatments. The ractopamine treatments were imposed when the gilts reached a BW of 85.7 kg and lasted for the duration of the final 4 wk until carcass data were collected. Lipids from the belly, outer and inner layers of backfat, and LM were extracted and analyzed for fatty acid composition from 6 pigs per treatment at wk 4 and 8. Feeding CLA increased (P < 0.02) G:F during the final 4 wk. Pigs fed added fat as either CWG or BT exhibited decreased (P < 0.05) ADFI and increased (P < 0.01) G:F. Adding ractopamine to the diet increased (P < 0.01) ADG, G:F, and final BW. The predicted carcass lean percentage was increased (P < 0.05) in pigs fed CLA or ractopamine. Feeding either 5% fat or ractopamine increased (P < 0.05) carcass weight. Adding fat to the diets increased (P < 0.05) the 10th rib backfat depth but did not affect predicted percent lean. Bellies of gilts fed CLA were subjectively and objectively firmer (P < 0.01). Dietary CLA increased (P < 0.01) the concentration of saturated fatty acids and decreased (P < 0.01) the concentration of unsaturated fatty acids of the belly fat, both layers of backfat, and LM. Ractopamine decreased (P < 0.01) the i.m. fat content of the LM but had relatively little effect on the fatty acid profiles of the tissues compared with CLA. These results indicate that CLA, added fat, and ractopamine work mainly in an additive fashion to enhance pig growth and carcass quality. Furthermore, these results indicate that CLA results in more saturated fat throughout the carcass.

Several transcription factors are involved in regulating lipid metabolism in various tissues of animals. Adipocyte determination and differentiation-dependent factor 1 (ADD1), peroxisome proliferator activated receptor alpha (PPAR alpha), and peroxisome proliferator activated receptor gamma (PPAR gamma) regulate both lipogenesis and fatty acid oxidation. We determined the tissue distribution and genetic difference in mRNA concentrations of these transcription factors in two genetic populations of pigs (Newsham XL-sired Newsham Landrace x Large White Duroc and Duroc-sired US Yorkshire x Duroc-Landrace). We also determined the tissue distribution and genetic difference in the mRNA concentration of fatty acid synthase (FAS) and acyl-CoA oxidase (ACO). Our data showed that ADD1 was highly expressed in adipose tissue and liver and that mRNA concentrations of ADD1 were similar between the two genotypes. The PPAR alpha mRNA concentration was high in adipose tissue and was similar between the two genotypes. In both populations, PPAR gamma mRNA was detected only in adipose tissue. There was no difference between the two genotypes in PPAR gamma mRNA concentration. The ACO mRNA was expressed in adipose tissue, skeletal muscle, and liver with no difference between genotypes. The FAS mRNA concentration in adipose tissue was seven times higher than that in the liver. There was no detectable FAS mRNA in skeletal muscle. These data support the concept that pig adipose tissue has considerable capability for fatty acid oxidation and synthesis. The uniqueness of expression patterns for FAS and ADD1 mRNA further indicates that adipose tissue is significantly involved in fatty acid and triacylglycerol synthesis in pigs.

Adiponectin is an adipocyte-derived hormone that has been implicated recently in the regulation of inflammation in immunocytes, and in lipid metabolism and glucose homeostasis in liver, skeletal muscle and adipocytes. However, information in non-rodent models is limited. We have cloned and sequenced the porcine adiponectin open reading frame and evaluated the regulation of adiponectin in vivo following lipopolysaccharide (LPS) or E. coli administration. The porcine sequence shares approximately 88, 86, 85 and 83% homology with the dog, human, cow and mouse adiponectin respectively, and 79-83% similarity with dog, human, cow and mouse proteins at the amino acid level, based on the translated porcine sequence and GenBank submissions for the other species. Relative serum adiponectin concentrations were not altered in pigs infused with E. coli, and mRNA expression in adipose tissue was not responsive to LPS. However, analysis of serum from very lean vs a substantially fatter genotype of pig indicated that relative circulating adiponectin concentrations are higher (P,0·01) in the lean pigs than in the fatter genotype, and that the difference is established relatively early in the growth curve. Also, incubating pig adipocytes for 6 h with recombinant pig adiponectin resulted in an approximately 30% reduction (P,0·05) in lipogenesis compared with adipocytes under basal conditions and with those incubated in the presence of insulin. This is the first report in any species that adiponectin antagonizes the incorporation of glucose carbon into lipid in the adipocyte, and provides additional evidence that adiponectin acts as an autocrine regulatory factor to regulate energy metabolism.

An experiment was conducted to determine the efficacy of dietary conjugated linoleic acid (CLA) as a growth promotant in weanling swine. Weanling pigs (n = 192; 7.6 kg and 29 d of age) were randomly assigned to four treatments that were arranged as a 2 x 2 factorial. Concentrations of dietary CLA (0 or 0.6%) and antibiotics (+/-) constituted the main effect variables. Dietary CLA treatments consisted of a 1% addition of an oil containing 60% CLA isomers or 1% soybean oil, and dietary antibiotic treatments were antibiotics or no antibiotics. The experimental diets were fed for 9 wk in four phases (1, wk 1; 2, wk 2 and 3; 3, wk 4 through 6; and 4, wk 7 through 9), after which all pigs were fed identical medicated diets for the duration of the finishing phase. Live weights were recorded at wk 17 postweaning and at marketing to determine any residual effects of dietary treatments on finisher ADG and days to market. Medicated diets fed during phases 1 and 2 contained 55 mg carbadox/kg; during phase 3 contained 299 mg tilmicosin/kg; and during phase 4 contained 110 mg tylosin and 110 mg sulfamethazine/kg. Pigs fed medicated diets had higher overall ADG than pigs fed unmedicated diets for wk 0 through 9 (P < 0.03). Gain:feed (G:F) was greater for pigs fed medicated diets than for pigs fed unmedicated diets during phase 1 (P < 0.03) and for the duration of the nursery phase (P < 0.03). There were no effects of CLA on ADG, ADFI, or G:F. There were no residual effects of nursery CLA or antibiotics on finisher ADG and days to market. Blood samples collected from a subset of pigs (n = 72) at the completion of phases 2, 3, and 4 were assayed for serum IGF-I and antibody concentrations to porcine reproductive and respiratory syndrome virus (PRRSV) and Mycoplasma hyopneumoniae. There was a tendency for pigs fed medicated diets to have greater IGF-I concentrations than pigs fed unmedicated diets at the completion of phase 4 (P < 0.06). Pigs fed CLA had greater antibody titers (P < 0.02) to Mycoplasma hyopneumoniae at d 63 than pigs fed diets without CLA. These results indicate that feeding 0.6% dietary CLA did not enhance growth performance in weanling swine and that the use of dietary antibiotics can increase production efficiency in nursery pigs. Furthermore, there were no interactions between CLA and dietary antibiotics on the variables addressed in this study.

Soy protein regulates adiponectin and peroxisome proliferator-activated receptor alpha (PPARalpha) in some species, but the effect of dietary soy protein on adiponectin and PPARalpha in the pig has not been studied. Therefore, the objective of this study was to determine whether soya bean meal reduction or replacement influences serum adiponectin, adiponectin mRNA, serum metabolites and the expression of PPARalpha and other genes involved in lipid deposition. Thirty-three pigs (11 pigs per treatment) were subjected to one of three dietary treatments: (i) reduced crude protein (CP) diet containing soya bean meal (RCP-Soy), (ii) high CP diet containing soya bean meal (HCP-Soy) or (iii) high CP diet with corn gluten meal replacing soya bean meal (HCP-CGM) for 35 days. Dietary treatment had no effect on overall growth performance, feed intake or measures of body composition. There was no effect of dietary treatment on serum adiponectin or leptin. Dietary treatment did not affect the abundance of the mRNAs for adiponectin, PPARalpha, PPARgamma2, lipoprotein lipase or fatty acid synthase in adipose tissue. The mRNA expression of PPARalpha, PPARgamma2, lipoprotein lipase or fatty acid synthetase in loin muscle was not affected by dietary treatment. In liver tissue, the relative abundance of PPARalpha mRNA was greater (p < 0.05) in pigs fed the HCP-Soy diets when compared to pigs fed RCP-Soy or HCP-CGM diets. Hepatic mRNA expression of acyl-CoA oxidase or fatty acid synthase was not affected by dietary treatment. Western blot analysis indicated that hepatic PPARalpha protein levels were decreased (p < 0.05) in pigs fed the RCP-Soy diets when compared to pigs fed the HCP-Soy diets. These data suggest that increasing the soy protein content of swine diets increases hepatic expression of PPARalpha without associated changes in body composition.