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Evaluation of the effects of dietary fat, conjugated linoleic acid, and ractopamine on growth performance, pork quality, and fatty acid profiles in genetically lean gilts¹

T. E. Weber^*,2, B. T. Richert^*, M. A. Belury, Y. Gu, K. Enright^* and A. P. Schinckel^*,3

^* Department of Animal Sciences, Purdue University, West Lafayette, IN 47907; and Department of Human Nutrition, Ohio State University, Columbus 43210; and and Research Institute of Bastyr University, Kenmore, WA 98028.

	Abstract

Top Abstract INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
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.

Key Words: conjugated linoleic acid • dietary fat • fatty acid • pig growth • ractopamine

	INTRODUCTION

Top Abstract INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
The pork industry is constantly seeking economical methods that will increase production efficiency and carcass quality. Adding animal fats to swine diets enhanced G:F (Seerley et al., 1978; Stahly and Cromwell, 1979). It is also well known that the fatty acid composition of the pig reflects the fatty acid pattern of the diet (Ellis and Isbell, 1926; Warnants et al., 1999).

The use of the beta adrenergic agonist ractopamine increased growth rate, G:F, and carcass leanness (Stoller et al., 2003; Williams et al., 1994). Feeding ractopamine decreased fatty acid synthesis in porcine adipose tissue (Mills et al., 1990; Mersmann, 1998), which could alter the fatty acid composition of the adipose tissue. Furthermore, fatty acid synthase mRNA and ultimately fatty acid synthesis decreased in pigs treated with porcine somatotropin (Mildner and Clarke, 1991). Indeed, porcine somatotropin treatment altered the composition of fatty acids in adipose tissue and LM by increasing the abundance of unsaturated fatty acids (UFA; Ramsay et al., 2001). However, changes in the fatty acid composition of carcass tissues from pigs fed ractopamine have not been reported.

Adding CLA to swine diets reduced carcass fat (Dugan et al., 1997) and increased belly firmness (Eggert et al., 2001). Feeding CLA increased the abundance of SFA in porcine muscle (Joo et al., 2002), adipose tissue (Bee, 2000; Eggert et al., 2001), and bellies (Eggert et al., 2001). The current study was designed to determine whether ractopamine and rendered animal fats alter the fatty acid content of porcine carcasses and also to determine whether CLA can counteract the effects of ractopamine and dietary fat on the lipid content of carcass tissues.

	MATERIALS AND METHODS

Top Abstract INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Animals, Experimental Design, and Housing
A total of 228 genetically lean female pigs (Newsham XL sires x Duroc x Yorkshire Landrace dams; initially, 59.10 kg, SD = 3.0 kg) were randomly assigned (blocked by BW) to a 2 x 3 factorial arrangement consisting of dietary CLA and added fat treatments. The CLA treatment consisted of 1% of a commercially available CLA product containing 60% CLA isomers (0.6% CLA) or 1% soybean oil. Dietary fat treatments consisted of 1) diets containing 0% added fat, 2) diets containing 5% choice white grease (CWG), or 3) diets containing 5% beef tallow (BT). After a period of 4 wk (phase 1), when the average BW reached 85.67 kg (SD = 5.0 kg), the pigs were further allocated to receive diets containing 10 ppm of the complete diet containing ractopamine hydrochloride or diets containing no ractopamine hydrochloride in a 2 x 2 x 3 factorial arrangement consisting of ractopamine level (0 or 10 ppm of complete diet), dietary CLA level, and added fat level (phase 2).

The pigs were housed in an all-in/all-out curtain-sided grower-finisher facility and reared in groups of 3 pigs per pen (1.8 m²/pig) except for one block that contained 7 pigs per pen (0.8 m²/pig) during the first phase (wk 0 to 4) of the experiment. At the completion of phase 1 (wk 0 to 4), a subset of the pigs (n = 48; 4 pigs per pen from a block containing extra pigs; 8 pigs per dietary treatment) was removed from the trial to obtain carcass and belly quality data and fatty acid profiles. Therefore, there were 10 replicate pens per dietary treatment for the first 4 wk of the trial and 5 replicate pens per treatment for the remainder of the growth trial (phase 2). All pigs had ad libitum access to feed and water through a one-hole self-feeder and a nipple waterer. The animal handling protocols were approved by the Purdue University Animal Care and Use Committee.

Experimental Diets and Growth Performance
All diets were formulated to meet or exceed the estimated nutrient requirements (NRC, 1998). The pigs were fed 2 dietary phases with phase changes occurring after 4 wk. Dietary treatments within each phase were formulated to contain equivalent lysine/ MCal of ME (Table 1). Diets containing CLA were formulated to provide 0.6% added CLA (1% of a product containing 60% CLA isomers (30.1% cis-9, trans-11; 31.4% trans-10, cis-12; and 0.02% trans-9, cis-11; Natural Lipids, Hovdebygda, Norway); the CLA oil was added at the expense of soybean oil. The fatty acid profiles of the supplemental fats and oils are presented in Table 2. For phase 2 diets containing ractopamine hydrochloride (Paylean; Elanco Animal Health, Indianapolis, IN), the ractopamine hydrochloride premix was added at the expense of corn. The pigs and feeders were weighed every 14 d to determine ADG, ADFI, and G:F.

Longissimus Muscle Quality Measurements
At 24 h postmortem, after a 15 min bloom, subjective measurements of LM color, marbling, and firmness were taken on the carcasses at the interface of 10th and 11th rib (NPPC, 1999). Water holding capacity was analyzed using the drip loss method (Rasmussen and Stouffer, 1996). Briefly, muscle samples were collected from one of the 2.5-cm chops using a 2.5-cm coring device. The samples (triplicate 7-g core samples/ chop) were then placed into the drip loss tubes so that the cut surface of the chop was perpendicular to the long axis of the drip loss tube. After 24 h at 4°C, the drip loss containers plus sample was reweighed. The muscle sample was then removed, and the container containing the exudates was reweighed. Therefore, the drip loss was calculated as the percentage of the mass of the original chop sample that the exudates represented.

Belly Firmness Measurements
At 24 h postmortem the portion of the belly anterior to the 10th rib was removed from the carcass and placed skin side down and centered horizontally over a 1-cm wide bar. Bacon length was analyzed as the length measured between the anterior and the posterior end of the belly when it was suspended over the bar. Therefore, firmer bellies would give greater values of the length measured between the anterior and posterior ends when suspended over the bar. Additionally, belly firmness scores (range 1 to 5) were assigned to the bellies; a score of 5 was assigned to the firmest bellies, and a score of 1 was assigned to the softest bellies. The scores were assigned by personnel with no knowledge of the dietary treatments.

Carcass and Belly Characteristics of the Subset of the Gilts Removed After Phase 1
The following measurements were taken on the subset (n = 48) of pigs that was slaughtered at the completion of the first phase of the experiment: HCW, backfat depth at the 10th rib, loin eye area, and belly firmness score. The procedures used to obtain these measurements were the same as those used to analyze the carcass quality of the pigs harvested at the completion of the trial, which were outlined previously.

Lipid and Fatty Acid Analysis
Samples of LM, belly, and inner middle and outer layers of subcutaneous backfat were collected and freeze-dried. Samples were stored and then extracted and prepared for gas chromatography all at once so that variation in method and instrumentation would be minimized. Lipids were extracted from freeze-dried tissue aliquots by the method of Bligh and Dyer (1959) with modifications as we have described (Eggert et al., 2001). Lipid concentrations (milligram lipid per gram dry weight of tissue) were quantified; then lipid extracts were frozen (–80°C). Fatty acid methyl esters were prepared by incubating extracts with tetramethylguanidine at 95°C (Shantha et al., 1993). Methyl esters were separated and quantified by gas–liquid chromatography using a 30-m Omega-wax 320 capillary column (Supelco Chromatography Products, Bellefonte, PA). Helium flow rate was 30 mL/min; oven temperature was 175°C for 4 min and increased to 220°C at a rate of 3°C/min. Identification of fatty acid methyl esters was accomplished by comparing retention times of peaks of unknown origin with peaks of retention times of authentic standards spiked with methyl esters of CLA isomers (c9t11-CLA, t10c12-CLA, c9c11-CLA, t9t11-CLA, Matreya Inc., Pleasant Gap, PA). Data were integrated using Chemstation Software (Packard Instrument Company, Meriden, CT). Iodine values (IOV) were calculated for the fatty acid composition of the various fat depots according to the AOAC (1990) equation: IOV = (% hexadecenoic acid x 0.950) + (% octadecenoic acid x 0.860) + (% octadecadienoic acid x 1.732) + (% octadecatienoic acid x 2.616) + (% eicosenoic acid x 0.785) + (% docosenoic acid x 0.723).

Statistical Analysis
Data were analyzed as a randomized complete block design using the GLM procedure of SAS (SAS Inst. Inc., Cary, NC). For the first phase of the experiment (wk 0 to 4), and for the subset of pigs that was slaughtered at the completion of phase 1, a 2 x 3 factorial arrangement consisting of the 2 CLA levels (0 and 0.6%) and the 3 fat levels (0%, CWG, and BT) was used. Performance data from the second phase of the trial (wk 4 to 8) and carcass data collected at the completion of the experiment were analyzed as a 2 x 2 x 3 factorial arrangement of treatments that included the level of ractopamine hydrochloride (0 or 10 ppm), the 2 levels of CLA treatment, and the 3 levels of dietary fat treatment. Pen served as the experimental unit for the performance and carcass data. Belly weights and belly lengths were used as covariates in the objective belly firmness analysis. The models included the effects of ractopamine, CLA, dietary fat treatments, and all 2- and 3-way interactions. The residual mean square error term was used as the error term to test the main effects and interactions. Means were evaluated using the PDIFF and STDERR options of GLM.

	RESULTS

Top Abstract INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
Growth Performance
Pigs fed diets containing 5% added fat had greater (P < 0.01) G:F for wk 0 to 2 and tended to have greater G:F for wk 2 to 4 than gilts fed diets containing 0% added fat (Table 3). Furthermore, feeding diets containing 5% added fat elicited an increase (P < 0.01) in G:F during the first phase (wk 0 to 4) of the experiment. Pigs fed diets containing ractopamine had greater (P < 0.01) ADG and G:F than pigs fed diets devoid of ractopamine during wk 4 to 6, wk 6 to 8, and during the entire period in which the ractopamine treatment was imposed (wk 4 to 8; Table 4). Pigs fed diets containing CLA had increased (P < 0.03) ADG during wk 4 to 6 and increased G:F wk 6 to 8 (P < 0.01) and wk 4 to 8 (P < 0.02). Pigs fed diets containing 5% added fat had decreased (P < 0.02) ADFI during wk 6 to 8 and wk 4 to 8 and, therefore, demonstrated greater (P < 0.01) G:F during the same periods than gilts fed diets containing 0% added fat. Pigs fed ractopamine had greater (P < 0.01) BW at the completion of the experiment than pigs fed diets devoid of ractopamine. Furthermore, feeding diets containing 5% added fat tended (P = 0.10) to increase final BW.

Fatty Acid Composition
After the first phase of the experiment (wk 4), bellies from pigs fed CLA had more (P < 0.01) total CLA, more SFA (P < 0.01), less MUFA (P < 0.01), and less total UFA (P < 0.01) than pigs fed no added CLA (Table 7). Likewise, the IOV of bellies from pigs fed CLA was decreased (P < 0.01). The fatty acid concentrations measured in the belly were altered by dietary CLA except 16:1n-7, 18:3n-6, 20:4n-6, and 20:5n-3. This is reflected by the lack of difference found in total PUFA content of the bellies from pigs fed CLA. Inner-layer backfat from pigs fed CLA for a period of 4 wk had more (P < 0.01) total CLA and decreased (P < 0.01) MUFA compared with pigs fed no added CLA (Table 8). Feeding fat in the form of BT increased (P < 0.01) the content of 18:3n-6 but did not alter the abundance of any other fatty acids from inner-layer backfat. For outer-layer backfat, the CLA content was increased (P < 0.01), and the abundance of MUFA was decreased (P < 0.01) by feeding CLA (Table 9). An interaction (P < 0.05) between CLA and dietary fat-type was found for 20:5n-3. Within the treatment group fed CLA, there was no difference between dietary fat-type for the abundance of 20:5n-3, but for pigs fed diets containing added CLA there was an increase (P < 0.05) in the abundance of 20:5n-3 in pigs fed CWG compared with pigs fed 0% added fat or CWG.

	DISCUSSION

Top Abstract INTRODUCTION MATERIALS AND METHODS RESULTS DISCUSSION LITERATURE CITED

 
The current study examined the effects of ractopamine, CLA, and rendered animal fats on growth performance, carcass characteristics, and fatty acid profiles of genetically lean pigs. As found in previous studies, both ractopamine (Williams et al., 1994; Stoller et al., 2003) and fat (Williams et al., 1994) increased ADG and G:F. Adding CLA to the diets increased ADG for a portion of the experiment (wk 6 to 8) and increased G:F during the second phase of the experiment. The increase in G:F agrees with other studies in which feeding CLA has been found to enhance G:F (Dugan et al., 1997; Ostrowska et al., 1999). The increase in G:F found in pigs fed CLA is likely due to a decrease in fat deposition and a corresponding increase in muscle protein accretion. In the current study, it was found that CLA tended to decrease backfat depth and increase LM area, but not significantly. Indeed, other investigators (Dugan et al., 1997; Swan et al., 2001) have found that feeding pigs diets containing CLA increased the weight of the LM.

Mechanistically, CLA may decrease adiposity of pigs through its ability to depress the activity of steroyl coenzyme A desaturase in porcine adipose tissue (Smith et al., 2002). Indeed, the increased abundance of saturated fatty acids found in the tissues of pigs fed CLA may be reflective of a decrease in desaturase activity. Furthermore, an increase in the expression of the stearyl-coA desaturase gene is associated with adipocyte hypertrophy (Smith et al., 1999). Another mechanism via which CLA may decrease adiposity in the pig is by the induction of adipocyte apoptosis. Feeding diets containing CLA to mice increased apoptosis in white adipose tissue (Miner et al., 2001). This apoptotic effect in mouse adipose tissue was attributed to consumption of the trans-10, cis-12 isomer of CLA (Hargrave et al., 2002). Treating 3T3-L1 adipocytes with CLA inhibited proliferation but stimulated the filling of the cells with lipid (Satory and Smith, 1999). The inhibition of adipocyte proliferation might have been due to apoptosis, but apoptosis was not measured. Additionally, treating the 3T3-L1 adipocytes with CLA increased the cellular content of palmitic acid, indicating that CLA stimulated de novo lipogenesis. It is interesting that in our study the abundance of palmitic acid was increased in the tissues of pigs fed CLA. This suggests that CLA may stimulate de novo lipogenesis in porcine tissues. However, further research is needed to determine whether CLA induces apoptosis and de novo lipogenesis in porcine adipocytes.

Feeding CLA made the fatty acid composition of the inner-layer backfat less resistant to the changes observed with animal-fat-supplemented diets. The pigs fed CLA had a greater increase in the magnitude of UFA when animal fats were added to the diets. This is intriguing given the findings that CLA typically decreased the content of UFA in porcine tissues (Eggert et al., 2001). It is possible that CLA stimulated lipid filling in this later maturing adipose depot. As previously discussed, treating adipocytes with CLA in vitro induced adipocyte differentiation (Satory and Smith, 1999). Given the high abundance of oleic acid in rendered animal fats, it is possible that excess dietary lipid may have been incorporated into adipocytes in inner layer adipose tissue when the pigs were fed CLA. However, more research is necessary to determine the effects of CLA on lipid filling in porcine adipocytes in the presence of UFA.

As found in previous studies, feeding ractopamine increased the lean content of pig carcasses (Williams et al., 1994; Stoller et al., 2003), but had relatively little effect on the fatty acid compostion of pig tissues when compared with the effects of CLA. As previously found (Stoller et al., 2003), ractopamine decreased the total lipid content of the LM, but did not affect subjective marbling scores. Feeding ractopamine increased the abundance of total UFA found in inner-layer back-fat, but did not alter the abundance of palmitic acid. The relative lack of a change in the fatty acid profiles is suprising given that ractopamine has been shown to decrease de novo lipogenesis in porcine adipocytes (Mills et al., 1990). Furthermore, we hypothesize that ractopamine induced reduction in lipogenesis would reduce the palmitic acid content of adipose tissue. These data suggest that feeding ractopamine had little effect on the fatty acid profiles of porcine tissues and that further research is necessary to characterize the effects of ractopamine on the fat metabolism of the pig.

The increased percent lean found in pigs fed ractopamine is likely due to both a reduction in adipose tissue accretion and a corresponding increase in muscle protein synthesis. As previously discussed, ractopamine inhibited lipogenesis in porcine adipose tissue (Mills et al., 1990). Recently, it has been noted that ß-adrenergic receptor agonists, including ractopamine, increased apoptosis in mouse adipose tissue (Page et al., 2004). Increased apoptosis in adipocytes may at least partially explain why pigs fed ractopamine generally have less body fat. However, more research is necessary to determine whether ractopamine induces apoptosis in porcine adipocytes. Furthermore, it has been shown that pigs fed ractopamine have an increase in muscle protein synthesis (Bergen et al., 1989; Adeola et al., 1992). Mechanistically, the increase in muscle protein synthesis may result from the increased myofibrillar gene expression found in pigs fed ractopamine (Grant et al., 1993). Further research is necessary to determine the cellular signaling mechanisms that ultimately lead to increased muscle protein synthesis in pigs fed ractopamine.

As found in other studies, feeding CLA (Eggert et al., 2001) or compounds containing CLA (O’Quinn et al., 2000) to growing and finishing pigs increased belly firmness. Likewise, we found that CLA increased the abundance of SFA, decreased the abundance of UFA, and decreased the IOV of pig belly tissue. The increased saturation of the belly tissue fatty acid profile may explain the increase in belly firmness noted in pigs fed CLA. Furthermore, we found that ractopamine tended to decrease belly firmness scores, but this trend was not observed in the hanging belly length measurements measure. Indeed, ractopamine might have slightly decreased the SFA content of belly tissue, but the effect of ractopamine on belly firmness and fatty acid content was small compared with the effect of CLA.

The results of this experiment indicated that CLA increased the SFA content of porcine tissues and enhanced carcass characteristics such as leanness and belly firmness in pigs fed ractopamine as well as pigs not fed ractopamine. Therefore, feeding CLA may be a nutritional means to maintain carcass quality and firmness when other management practices that alter carcass quality are used. Ractopamine had relatively little effect on the fatty acid composition of carcass tissues. The data presented herein also indicate that CWG and BT are essentially equivalent in terms of their effects on growth performance and carcass fatty acid composition.

	Footnotes

 
¹ The authors acknowledge the Fats and Proteins Research Foundation for financial support. Contribution No. 2004-17507 from the Purdue University Agricultural Experiment Station, West Lafayette, IN 47907.

² Current address: USDA/ARS Catfish Genetics Research Unit, Stoneville, MS 38776.

³ Corresponding author: aschinck{at}purdue.edu

Received for publication December 10, 2004. Accepted for publication October 17, 2005.

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