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ANIMAL PRODUCTS |
* Department of Animal Sciences, and
and
Department of Foods and Nutrition, Purdue University, West Lafayette, IN 47907;
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JBS United, Sheridan, IN 46069;
and
Adisseo USA Inc., Alpharetta, GA 30005
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Abstract |
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 Top Abstract INTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONIMPLICATIONSLITERATURE CITED |
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-tocopherol acetate) and fat supplementation on growth and carcass quality characteristics, oxidative stability of fresh and cooked pork patty in storage, fatty acid profiles of muscle and adipose tissue, and VE concentrations of plasma, muscle, and adipose tissue were studied. Six hundred pigs were allocated to 1 of 6 diets and fed for 63 d in a 3 x 2 factorial design. The dietary treatments included 3 fat levels (normal corn, high oil corn, high oil corn plus added beef tallow) and 2 levels of VE supplementation (40 IU/kg, normal VE supplementation; and 200 IU/kg, high VE supplementation). At 113 kg of BW, 54 pigs were slaughtered as a subsample to evaluate dietary effects on pork quality. Growth performance and meat quality characteristics did not differ (P > 0.05) among treatment groups. The high level of VE supplementation had a beneficial effect on the oxidative stability of pork as indicated by thiobarbituric acid reactive substance (TBARS) values. Lean tissue had lower (P < 0.05) TBARS in the group fed the high VE than in those fed the normal VE level. The TBARS values differed among storage periods (0 to 6 d) and also between fresh and cooked ground ham. Fat type did not significantly affect total saturated and unsaturated fatty acids proportions in the neutral and polar fraction of muscle. Adding VE acetate led to greater (P < 0.05) monounsaturated and total unsaturated fatty acid proportions in neutral lipids of muscle and adipose tissues. Increasing dietary levels of VE acetate increased the concentration of VE in plasma and muscle. These results indicate that dietary VE acetate supplementation increased (P < 0.05) lipid stability and the VE concentration of muscle.
Key Words: -tocopherol • fatty acid • high oil corn • lipid oxidation • pork • supplemental fat
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INTRODUCTION |
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TopAbstractINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONIMPLICATIONSLITERATURE CITED |
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; Adeola and Bajjalieh, 1997). Unfortunately, adverse pork quality can result from pigs consuming diets composed of supplemented fat, often high in PUFA (Gatlin et al., 2002). The added fat may be more susceptible to oxidation and lead to the development of off-flavors and loss of color and nutrient values (Pearson et al., 1983) and is a major problem in the development of new convenience meat products and processes (Gray and Pearson, 1987).
To alleviate the possibility of greater lipid oxidation in products from such feeding strategies, investigators have proposed adding antioxidants to high fat diets. Pearson et al. (1977) summarized the results of several attempts to increase lipid stability in meat by adding vitamin E (VE, -tocopherol acetate) to diets. Vitamin E is a membrane-associated antioxidant that can effectively protect the vulnerable unsaturated fatty acids in cell membranes and plasma lipoproteins from oxidizing agents, both endogenous and exogenous (McCay et al., 1971; Diplock and Lucy, 1973). Incorporation of tocopherol into the lipoprotein matrix of cell membranes can maintain cellular integrity and protect unsaturated fatty acids (USFA) from oxidation by free radicals (Tappel, 1962).
The amount and type of USFA in the tissues, as well as the relative abundance of pro- and antioxidants influence the susceptibility of meats to lipid oxidation (Monahan et al., 1993; Gatellier et al., 2000). Therefore, the source of fat in the diet and the amount of dietary VE will affect the oxidative stability of muscle and adipose tissue. Dietary VE supplementation in finishing diets may offer an effective means for incorporating an antioxidant in cell membranes, which would stabilize tissues containing elevated levels of USFA (Buckley et al., 1989; Monahan et al., 1992). Feeding pigs HOC and beef tallow is a common practice in the industry. However, little or no information is available regarding the effects of VE on pork quality characteristics when pigs are fed high oil diets (HOC or HOC plus fat, or both). Therefore, the objective of this research was to evaluate the effects of VE supplementation on pork quality in pigs fed high oil diets.
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MATERIALS AND METHODS |
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TopAbstractINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONIMPLICATIONSLITERATURE CITED |
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All animal handling protocols were approved by the Purdue Animal Care and Use Committee. Six hundred pigs (300 barrows and 300 gilts) were assigned to 1 of 6 dietary treatments in a 3 x 2 factorial design for 63 d, 2 pens of 25 pigs/sex/treatment combination. Treatments consisted of: normal corn (NC), HOC, and HOC plus fat (4% choice white grease) at 2 levels of VE supplementation (40 IU/kg, normal VE supplementation; and 200 IU/kg, high VE supplementation). The source of VE used in this study was DL-alpha tocopheryl acetate (Microvit E Promix 50, Adisseo, Alpharetta, GA). The calculated average crude fat levels in the 3 different basal diets (NC, HOC, HOC+fat) were 3.4, 6.3, and 10.1%, respectively. Lysine contents in the basal diets were 0.83% from 68 to 91 kg and 0.68% from 91 to 113 kg, and all diets were formulated to meet or exceed all nutrient requirements of the pigs (NRC, 1998). Levels of VE in the feed were verified analytically by Adisseo.
Slaughter and Processing Procedure
At 113 kg of BW, 9 barrows from each treatment combination were transported to the Purdue University Meat Science Research and Education Center for processing. Randomly selected barrows (3 per treatment), 1 or 2 per pen, were slaughtered on each of 3 slaughter days, using standard accepted processing procedures. All carcasses were scalded, dehaired, and placed in a chill cooler (4°C). At exsanguination, blood samples were collected into heparinized tubes, and plasma was recovered. Plasma samples were stored at –20°C for later processing and analysis.
Longissimus muscle pH values were recorded adjacent to the last rib at 45 min postexsanguination using a Beckman 
10 ISFET pH meter with a spear-tipped KCl gel probe (Fullerton, CA) that compensated for temperature differences. The pH meters were calibrated before and after measurement of every 4 carcasses using pH 4.00 and pH 7.00 buffers at 37°C. Probes were cleaned after each measurement by sequentially soaking in 10% bleach (vol/vol) and 10% pepsin (0.1 g/mL; Fisher Scientific, Pittsburgh, PA) solutions for 10 min each. Probes were inserted approximately 4.5 cm lateral to the midline of the carcass to a depth of approximately 5 cm at an angle perpendicular to the long axis of the LM to ensure measurements were taken near the center of the muscle.
At 24 h postexsanguination, carcasses were ribbed and ultimate muscle pH values were taken using the aforementioned equipment and procedures. Chilled carcasses were fabricated into primals and hams were vacuum packed and frozen at –20°C. Loins were further fabricated into 2.54-cm chops, and 2 chops from the center of the loin between the eighth and 10th rib were vacuum packaged and frozen at –20°C for later VE analyses and fatty acid profiles.
Pork Quality Evaluation
Classical meat quality data (color, marbling, firmness) were collected from the loin muscle adjacent to the 10th rib according to published pork quality standards (NPPC, 1991). Objective color measurements were determined on one 2.54-cm chop using a Hunter Lab 45°/0° D25-PC2
Colorimeter (Hunter and Associates Laboratory Inc., Reston, VA). Mean CIE-L* (lightness), a* (redness), and b* (yellowness) values were collected from 3 locations on the surface of each chop.
Water-holding capacity was determined on another chop from the 11th and 12th rib using the drip loss method (Rasmussen and Stouffer, 1996). Briefly, muscle samples were collected from one of the 2.54-cm chops (approximately 7.0 g) using a 2.54-cm-diam. coring device. Samples were placed into sealed drip loss tubes so that the cut surface of the meat was perpendicular to the long axis of the drip loss tube. Drip loss analysis was evaluated in triplicate from the core samples. After 24 h at 4°C, the drip loss containers plus sample were reweighed. Muscle samples were removed, discarded, and the containers were reweighed with the exudates. Percentage drip loss was calculated and recorded.
Measurement of Lipid Oxidation
Hams were thawed and dissected to approximately 90% lean. Lean tissue was coarse ground (a 0.6-cm plate), and 2% salt was added and thoroughly mixed. The ground ham was uncured. Lean was then reground through a 3-mm plate, and patties (approximately 12 cm diam. and 114 g) were made at 4°C. Four patties were randomly selected for lipid oxidation studies. Two patties were placed in polystyrene trays and overwrapped with an oxygen-permeable PVC meat stretch-wrap (O2 transmission rate: 6,000 to 8,000 mL of O2/m2 per 24 h at 1 atmosphere, 23°C, and 75% relative humidity) and stored at 4°C under fluorescent lighting.
At 0, 2, 4, and 6 d of storage, 10 g were collected from each patty and analyzed for lipid oxidation. Two additional patties were sealed in 30 x 18 cm retortable vacuum bags and placed in hot water bath and cooked to an internal temperature of 70°C for 30 min. Samples were cooled, overwrapped with the aforementioned film, and stored at 4°C under fluorescent lighting and sampled at 0, 2, 4, and 6 d of storage. The time from slaughter to cook (time 0) was approximately 26 h.
Lipid oxidation in the ham samples was assessed by the thiobarbituric acid (TBA) distillation method (Tarladgis et al., 1960). A minced sample (10 g) was placed in a 50-mL test, blender cup and homogenized with 50 mL of deionized distilled water using a Sorvall Omni Mixer (Model 17105, Dupont Instruments, Newtown, CT) for 2 min at high speed (speed setting 7). Butylated hydroxytoluene [0.2 mL of a solution containing 1.5 g of butylated hydroxytoluene (BHT) in 10 mL of 100% ethanol] was added before the blending step to prevent autoxidation.
The meat slurry was transferred to a round-bottom boiling flask (300 mL). Five boiling beads and approximately 1.0 mL of Antifoam Emulsion A (Sigma Corporation, St. Louis, MO) were added. The blender cup was rinsed with 50 mL of 5% hydrochloric acid, and then the rinsing fluid was added to the boiling flask. Meat slurry was boiled on heaters until 50 mL of distillate was collected. After cooling, 5 mL of distillate was transferred to a test tube (13 x 100 mm), and TBA solution (5 mL) was added. The mixture was vortexed and then boiled in a water bath for 35 min to develop color. After cooling for 10 min in cold water, absorbance was recorded on a spectrophotometer (Beckman Instruments Inc., Fullerton, CA) at 538 nm. Absorbance values were multiplied by 7.8 to obtain TBA values. Malonaldehyde standard curves were prepared by making appropriate dilutions of 1, 1, 3, 3-tetraethoxy-propane (Sigma) standard solutions. Thiobarbituric acid-reacting substances (TBARS) values were calculated from the standard curve and expressed as milligrams of malonaldehyde equivalents per kilogram of tissue.
Fatty Acid Profiles
For fatty acid determination, loin tissue (0.5 g, ground to a powder in liquid nitrogen) or subcutaneous fat tissue (0.3 g, diced) was mixed in 2 mL of methanol; then 4 mL of chloroform was added. After storing at 4°C for 30 min, 1 mL of 2 M KCI was added and centrifuged at 228 x g for 7 min at 4°C in a Beckman J2-HS centrifuge (Beckman Instruments Inc., Palo Alto, CA). The bottom chloroform layer was transferred to another test tube, and the extraction was repeated as described previously. The chloroform was then eliminated by N2 gas evaporation.
Dried samples were reconstituted in 2 mL of hexane:MTBE (tert-butyl ether, 200:3), and the samples were loaded onto SPE cartridges (Fisher Scientific SPE cartridge, PrepSep columns). Neutral lipids were collected with 12 mL of MTBE:acetic acid (100:0.2) solution, and polar lipids were collected with 12 mL of MTBE:methanol:ammonium acetate (10:4:1). All the eluate was transferred to acid-washed tubes. Samples were dried under nitrogen at 50°C, and 2 mL of tetra-methylguanidine (Fisher Scientific, Pittsburgh, PA) in methanol (1:4, v:v) was added. Tubes were capped tightly and heated in a boiling water bath for 10 min. After cooling to room temperature, 10 to 15 mL of saturated NaCl solution was added.
Esters were extracted with 6 to 8 mL of petroleum ether and then centrifuged at 228 x g for 5 min at 4°C. The upper petroleum ether layer was transferred to another tube, and the extraction was repeated as described previously. The petroleum ether was then eliminated by N2 gas evaporation. Dried samples were reconstituted in 1.5 mL of hexane, vortexed, and centrifuged at 228 x g for 5 min at 4°C. The clear portion of the sample was extracted and placed into Target DP, glass, gas chromatography (GC) vials with polypropylene caps (Fisher Scientific). The samples were stored at –80°C for GC analysis. An antioxidant (BHT) was added (0.01%) to all solvents used for homogenization.
After fatty acid extraction, total fatty acids were analyzed using GC. A Hewlett-Packard (HP) 5890 series II, gas, capillary, gas-liquid chromatography equipped with a flame ionization detector, HP Chemstation, and autosampler (Hewlett-Packard Co., Palo Alto, CA) was used. An Omegawax 320 capillary column (Supelco Inc., Bellefonte, PA; 30 m x 0.32 mm x 0.25 µm) was used, with helium as the carrier gas. An initial oven temperature (175°C) was maintained for 4 min and then increased at 3°C per min to a final temperature of 220°C. This final temperature was held for 15 min. The total gas chromatographic run was 34 min for lean and fat tissue. All samples were introduced by split injection (1:33). Fatty acid identification was achieved by comparing retention times with an animal source standard (lard, Supelco). Fatty acid proportions are presented as area percentages.
Determination of VE
Vitamin E, as -tocophorol, was determined in the plasma, loin, and adipose tissue samples. Sample extraction was performed as described by Bieri et al. (1979) and Buttriss and Diplock (1984). Approximately 1 g of muscle or fat samples was homogenized in 5 vol of isotonic KCl with a glass-Teflon homogenizer to obtain whole tissue homogenates. A 1-mL aliquot of tissue homogenate was mixed with 1.0 mL of ethanol containing 20 µg of BHT/mL and 1 mL of 25% ascorbic acid. Twenty-five µL of 100 µM 
-tocopherol was added as the tocopherol internal standard. The samples were flushed with N2, preinculated at 70°C for 5 min in glass-stoppered centrifuge tubes, and 0.3 mL of 10 N potassium hydroxide was added followed by further incubation for 30 min. The tubes were cooled by placing in an ice bath. One milliliter of distilled water and 4 mL of purified hexane were added to the tubes, which were then vortexed for 1 min. The hexane layer was removed after 10 min of centrifugation (272 x g) and transferred to another vial.
After drying the hexane under N2, the residue was resuspended in 250 µL of ethanol containing 20 µg of BHT/mL. An aliquot was then injected into the HPLC for tocopherol analysis. Tocopherols were separated by HPLC at 1.0 mL/min using a reverse phase LC-18-DB column (25 cm x 5 mm, 5 µm particle size; Supelco, Bellefonte, PA). The column was equilibrated in a mobile phase (buffer A) composed of 50 mM sodium perchlorate in a mixture of ethanol:methanol:water (9.1:0.4:0.5). The VE was gradient-eluted with 100% ethanol containing 50 mM sodium perchlorate (buffer B). Monitoring was performed simultaneously with an electrochemical detector (amphoteric, 0.7V, BioAnalytical Systems, West Lafayette, IN) for VE (Pascoe et al., 1987) and UV detector (294 nm) for VE acetate. A 250-µL internal standard (-tocopherol) was included in all sample extractions to adjust for recovery. Identification and quantification of VE were accomplished by comparison of retention time as well as peak areas with -tocopherol standards.
Statistical Analysis
Data were analyzed using the GLM procedure of SAS (SAS Inst. Inc., Cary, NC). All means presented are least squares means of each group and SEM, together with the significance levels of the main effects of diet and VE levels, and the interaction between them. Treatment mean differences were tested with the Student-Newman-Keul’s test procedure. Significance was declared at P < 0.05, and a trend was assumed at 0.05 < P > 0.10. Final BW was used as a covariate in the analysis of carcass data. Sex effect was included in analysis of the growth data. No interaction between sex and dietary treatments was found, and so these interactions were removed from the final statistical model for growth. Lipid oxidation, quantified by the amount of TBARS, was analyzed using a repeated-measures model that included the fixed effect of treatments and storage time (0, 2, 4, and 6 d) as the repeated measure. Pen served as the experimental unit for growth performance data, and individual pigs were used as the experimental unit for pork quality data.
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RESULTS AND DISCUSSION |
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TopAbstractINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONIMPLICATIONSLITERATURE CITED |
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No differences in average daily gain were detected among treatments (Table 1). However, ADFI and feed conversion (G:F) differences were evident among dietary fat levels. These results disagree with the results of Asghar et al. (1991b), who observed improved average daily gain and feed efficiency when pigs received diets supplemented with 100 and 200 IU of VE/kg of feed during the early growth period (0 to 4 wk, initial weight 29 kg). Others, however, reported no differences in performance characteristics of pigs supplemented with VE over the weight range used in this study (Chung et al., 1992; Hoving-Bolink et al., 1998; Corino et al., 1999). Increased dietary energy concentration by feeding HOC or HOC+fat decreased ADFI (P < 0.05) by 7% and increased G:F (P < 0.04) by 8% over the NC treatment. The reduction in ADFI and improved G:F are similar to other results with finishing pigs fed diets with elevated energy concentrations (Adeola and Bajjalieh, 1997; Pettigrew and Moser, 1991).
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; Onibi et al., 2000). However, backfat tended (P = 0.09) to be greater in pigs supplemented with fat. This is in general agreement with the summary by Pettigrew and Moser (1991), who reported that backfat tended to increase with increasing fat supplementation. These data suggest that the amount of fat added to the diets tended to create a compositional difference in fat deposition. Pork Quality
Adding fat or VE had no effect on meat quality characteristics (Table 1
). The pH at 45 min postmortem of different diets ranged between 6.21 to 6.30, whereas ultimate muscle pH ranged between 5.67 to 5.73. Monahan et al., (1990) reported no differences in ultimate muscle pH of pork chops from pigs fed 3 levels of VE (10, 100, 200 IU/kg of feed). In addition, Cannon et al. (1996) and Hoving-Bolink et al. (1998) reported no effect of VE supplementation on pork quality characteristics.
Hunter color values (lightness, L*; redness, a*; yellowness, b*) of pork chops were not influenced (P > 0.05) by dietary VE and fat supplementations (Table 1). These data generally agree with earlier reports (Cannon et al., 1996; Zanardi et al., 1999; Swigert et al., 2004) where no effects of VE were observed on these instrumental color scores in meat from animals supplemented with vitamin E.
In agreement with the Hunter color data, the NPPC color, marbling, and firmness scores revealed little difference among treatment groups. Enhanced meat color through VE-supplementation has been demonstrated in beef (Faustman et al., 1989; Sherbeck et al., 1995) and lamb (Wulf et al., 1995). However, conflicting results exist relative to the effects on pork color stability (Monahan et al., 1992; Monahan et al., 1994; Lanari et al., 1995; Houben et al., 1998; Phillips et al., 2001). In the current study, no differences in objective or subjective color values were observed at 24 h postmortem. A readily apparent explanation for the inconsistent effect on color is not available. Asghar et al. (1991b) and Monahan et al. (1992) attributed the increase in color stability by enhanced VE supplementation to be partially due to improved marbling traits. Phillips et al. (2001) indicated that a possible explanation for no influence on color may be related to glycolytic muscle fibers, which do not absorb as much VE as oxidative fibers and are less responsive to the antioxidant effect of VE. Alternatively, the greater amount of PUFA present in pork may make it more susceptible to lipid and color oxidation, thereby overwhelming the antioxidant capabilities of VE. However, given that we did not evaluate color stability over time, this discrepancy is not surprising.
Pork chops from pigs fed different levels of fat exhibited no difference in drip loss, but dietary VE supplementation tended (P = 0.10) to reduce the drip loss. It has been reported that greater VE supplementation can have a positive effect on drip loss (Asghar et al., 1991b; Onibi et al., 2000). However, conflicting results were reported by others (Cannon et al., 1996; Jensen et al., 1997; Corino et al., 1999). In the current study, a lack of effect of VE on drip loss could be due to the variability in fat response to the VE supplementation. Drip loss was unaffected by dietary fat levels. However, VE supplementation tended (P < 0.10) to lower drip loss across all dietary fat sources.
Lipid Oxidation in Fresh and Cooked Pork
Feeding NC, HOC, and supplemented fat did not affect lipid stability in fresh product (Table 2). In the current study, salt was added to samples for to enlarge the extent of lipid oxidation. Therefore, the observed TBARS values for all storage periods were high when compared with those reported by other authors. In the cooked product, there was a tendency for an interaction (P < 0.07) between dietary fat level and high VE supplementation for d 0 TBARS values. The high VE supplementation decreased TBARS values in the NC and HOC+fat treatments but had no effect in the HOC treatment. At d 2, increased dietary fat in the HOC and HOC+fat treatment increased TBARS values 14% over the NC treatment (P < 0.005), and at d 6 the increased fat diets tended (P < 0.09) to have increased TBARS values over the NC dietary treatment. However, TBARS values were lowest (P < 0.05) in pork from pigs supplemented with the greatest level of VE (Table 2). These data show that pigs fed VE-enriched diets yield products with greater lipid stability and suggest that VE may be acting to inhibit oxidation at the tissue level. Jensen et al. (1997) and Monahan et al. (1990) showed that dietary supplementation improved the lipid stability in raw and cooked pork samples stored at 4°C for up to 8 d. Other investigations have also reported an effect of dietary VE on lipid oxidation in pork tissue (Asghar et al., 1991a; Buckley et al., 1995; Kingston et al., 1998). Monahan et al. (1990) reported that dietary supplementation with VE improved the oxidative stability of raw and cooked meat after refrigerated storage (4°C) up to 8 d. Cannon et al. (1996) also observed that the combination of dietary VE supplementation and vacuum packaging could minimize lipid oxidation during extended periods of storage and retail display. Houben et al. (1998) reported that meat from VE-supplemented pigs was more resistant to lipid oxidation when meats were stored for 10 d at 7°C in an illuminated retail display cabinet.
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; Gray and Pearson, 1987). Moreover, the addition of salt to the ground ham samples likely acted as a prooxidant in the system.
Storage time dramatically affected (P < 0.05) TBARS values. Degree of lipid oxidation increased as the storage time increased. Dirinck et al. (1996) reported that this oxidation process speeds up with the storage due to cell membrane lysis. Lipid oxidation during storage of the cooked state was greater (P < 0.05) compared with the fresh state at different storage periods. Heat treatment changes the oxidative stability of pork, and phospholipid oxidation present in subcellular membranes proceeds at a much greater rate during chill storage of cooked pork.
These data suggest that VE supplementation to growing pigs can protect resulting pork products from oxidation and can therefore improve shelf stability and product quality. Monahan et al. (1990) reported that dietary supplementation with VE significantly improved the oxidation stability of raw and cooked lean after 8 d of storage. Corino et al. (1999) reported that high levels of VE supplementation (300 mg/kg) in the last 60 d of pig finishing diets can reduce the production of TBARS. Generally, biological membranes are rich in polyunsaturated phospholipids and are in close contact with pro-oxidants. These membranes are very susceptible to peroxidation and lipid oxidation, which begins in raw meat (Gray and Pearson, 1987). Accumulation of VE in muscle tissue delays lipid oxidation and enhances the stability of membrane lipids (Asghar et al., 1989).
Fatty Acid Profiles
Fatty acid profiles of the neutral lipid fractions of pork muscles in relation to fat content and VE level are presented in Table 3. A VE x fat source interaction (P < 0.05) was observed where the proportion of palmitic (C16:0) acid was decreased in NC diet by feeding high levels of VE, which attributed to the decrease of saturated fatty acid (SAFA). However, at 200 IU, VE had no effect on C16:0 and SAFA when pigs were fed HOC or HOC+fat. There was a greater percentage of C18:1n9 (P < 0.001) and C22:5 (P < 0.02) with a tendency (P < 0.11) for a decrease of C16:1 in the tissues of the high VE treatment. Because oleic and palmitic acids are the main fatty acids of the neutral lipid fraction, these results suggest that VE supplementation to a NC diet can effectively change the tissue fatty acid profiles by increasing or protecting the oxidation of MUFA (P < 0.008). Treatments with NC as the basal diet also had greater proportion (P < 0.007) of C18:0 compared with other dietary fat treatments. In neutral lipids, the MUFA are the most abundant (50.0 to 53.4% of the total fatty acids), followed by the SAFA. The amount of MUFA was increased by feeding high level of VE (P < 0.05). These data show that supplementation of VE to the NC can decrease (P < 0.05) the proportion of SAFA and increase (P < 0.05) total percentage of USFA and unsaturated fatty acids:saturated fatty acids ratio (U:S; P < 0.05), whereas VE effects in the HOC and HOC+fat diets are not as prominent. Similar results were reported by Fuhrmann and Sallmann (1996) and Rey et al. (2001). The possible mechanism for this phenomenon may involve modulation of -9 desaturase activity by VE (Okayasu et al., 1977). Perhaps the increased enzyme activity by VE is related to peroxide-scavenging enzyme activity, which could reduce USFA oxidation. In addition, desaturase may convert stearoyl COA to oleoyl COA through a -9 double bond insertion. As a result, a variety of unsaturated fatty acids could be formed from oleate by the combination of elongation and desaturation reactions.
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noted that the neutral lipid fraction isolated from the L. dorsi muscle of pigs receiving the tallow diet had greater C16:0 and C18:1 and a lower proportion of C18:2 than similar fraction isolated from pigs receiving the soya oil diet. Lauridsen et al. (2000) and Nuernberg et al. (2002) observed that supplementation of VE changed fatty acid composition of mitochondria of the psoas major muscle and LM, respectively. In contrast, other studies found that dietary VE supplementation did not influence the fatty acid composition in the muscle tissue of pigs (Monahan et al., 1992; Onibi et al., 1998; Bosi et al., 2000).
The polar lipids fraction isolated from the loin muscle was influenced by diet and VE supplementation (Table 4). Supplementation of VE tended (P < 0.06) to reduce the proportion of C18:1n9 in NC- and HOC-based diets. The NC diets supplemented with 200 IU/kg of VE had a greater (P < 0.05) percentage of C16:0 than NC with 40 IU/kg of VE treatment. In contrast, lower proportion of C18:1n7 (P < 0.004) and C20:4 (P < 0.03) were observed in the NC and HOC-200 IU of VE supplemented group than the NC and HOC-40 IU of VE treatments with 200 IU of VE increasing these lipids in the HOC+fat treatment. The amount of SAFA (P < 0.01) increased with elevated VE under the NC treatment, whereas SAFA lipids decreased with elevated VE under the HOC and HOC+fat treatments. In contrast, the USFA (P < 0.02) and U:S (P < 0.03) decreased with 200 IU/kg of VE in the NC treatment and USFA increased with no change in U:S with elevated VE under the HOC and HOC+fat treatments. These data suggest that the changes of fatty acid profiles of the polar lipid fraction in muscle primarily occur in NC-based diet supplemented with VE. The proportion of PUFA was much greater and the proportion of MUFA was lower in the polar lipids than in the neutral lipid of muscle. These results are in agreement with Leseigneur-Meynier and Gandemer (1991) and Lauridsen et al. (1999). Rey et al. (2001) reported that alpha-tocopheryl acetate supplementation increased MUFA in polar lipids and suggested that it was correlated with -9 desaturase activity. Our results showed that the effect of dietary VE supplementation on fatty acid profiles were most observed in the neutral lipid fraction of NC-based diet. In our study, the effect of VE on the polar lipid fraction of muscle tissue was influenced by the dietary fat content.
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. The percentages of C16:0, C16:1, C18:0, and C18:1n7 decreased (P < 0.05) in HOC and HOC plus fat treatments compared with NC treatments. However, increased VE supplementation tended (P < 0.07) to decrease C18:1n7 in the NC treatment and increase this lipid in the HOC and HOC+fat treatments. Adipose tissue from pigs fed HOC and HOC+fat had a greater (P < 0.05) percentage of C18:2 than groups fed the control diet. The degree of saturation was greater (SAFA; P < 0.05) in pigs fed NC than in HOC and HOC plus fat treatment groups. Conversely, PUFA (P < 0.001), USFA (P < 0.002), and U:S (P < 0.004) were greater in HOC and HOC plus fat treatmenats. Supplementation with 200 IU/kg of VE increased (P < 0.05) the percentage of C18:1n9, MUFA, USFA, and U:S but lowered (P < 0.05) SAFA in adipose tissue. Increased VE supplementation decreased C14:0 (P < 0.01) and C18:3 (P < 0.03) in the NC and HOC treatments but increased these lipids in the HOC+fat treatment. Supplementation with 200 IU of VE also tended to increase C20:1 (P < 0.07) and decrease C16:0 (P < 0.06) and C20:5 (P < 0.08). Supplementation with VE appeared to affect the fatty acid profiles of subcutaneous fat, even though there was no significant increase in VE content of adipose tissue (Table 6). However, some have shown that dietary VE supplementation did not influence fatty acid composition in adipose tissue of pigs (Monahan et al., 1992; Onibi et al., 1998; Bosi et al., 2000). Thus, the effectiveness of VE may not only be affected by dietary concentrations of VE but also by fatty acid profile of the diet. Also, these results collectively show the effects of dietary fat composition (HOC and HOC+fat vs. NC) on adipose tissue fatty acid profiles. These observations are consistent with others who have reported that feeding elevated levels of USFA results in a marked increase in USFA in adipose tissue of pigs (Madsen et al., 1992; Chung et al., 1998; Rentfrow et al., 2003).
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Supplementation of dietary VE increased (P < 0.001) plasma and muscle tissue VE concentration. However, the concentration of VE in the adipose tissue was not influenced by increased VE supplementation. Given that VE is fat-soluble, we expected to observe greater VE in adipose tissue. The reason for lack of effect is not readily apparent given our plasma and muscle tissue VE concentrations were similar to those reported previously (Monahan et al., 1992; Pfalzgraf et al., 1995; Rey et al., 2001).
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IMPLICATIONS |
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TopAbstractINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONIMPLICATIONSLITERATURE CITED |
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Footnotes |
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2 Current address: Cargill Animal Nutrition, Minneapolis, MN 55440.
3 Current address: AusGene International, LLC, Gridley, IL 61744.
4 Corresponding author: dgerrard{at}purdue.edu
Received for publication August 22, 2005. Accepted for publication February 7, 2006.
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LITERATURE CITED |
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TopAbstractINTRODUCTIONMATERIALS AND METHODSRESULTS AND DISCUSSIONIMPLICATIONSLITERATURE CITED |
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J. K. Apple, C. V. Maxwell, D. L. Galloway, C. R. Hamilton, and J. W. S. Yancey Interactive effects of dietary fat source and slaughter weight in growing-finishing swine: III. Carcass and fatty acid compositions J Anim Sci, April 1, 2009; 87(4): 1441 - 1454. [Abstract] [Full Text] [PDF]
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Q. Guo, B. T. Richert, J. R. Burgess, D. M. Webel, D. E. Orr, M. Blair, A. L. Grant, and D. E. Gerrard Effect of dietary vitamin E supplementation and feeding period on pork quality J Anim Sci, November 1, 2006; 84(11): 3071 - 3078. [Abstract] [Full Text] [PDF]
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