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* Unité Mixte de Recherches Veau-Porc INRA-ENSAR, 35 590 Saint-Gilles, France and
and
Division of Food Animal Science, Department of Clinical Veterinary Science, University of Bristol, Langford, Bristol BS40 5DU, U.K.
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Abstract |
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0.4 in all groups and tissues, which is close to the recommended value for the entire diet of humans, as well as a robust decrease in the n-6:n-3 ratio. The decrease (P < 0.01) in the percentage of oleic acid in adipose tissue of pigs fed the linseed diet for 60 d could be attributed to a 40% decrease (P < 0.001) in stearoyl-CoA-desaturase activity. Diet did not (P > 0.05) affect the activities of acetyl-CoA-carboxylase, malic enzyme, or glucose-6-phosphate-dehydrogenase in any tissues. Muscle vitamin E content was decreased (P < 0.001) 30% in pigs fed crushed linseed for 60 d, whereas lower (P < 0.001) concentrations of skatole in pork fat were observed in linseed-fed pigs at all slaughter times. Inclusion of linseed (flaxseed) in swine diets is a valid method of improving the nutritional value of pork without deleteriously affecting organoleptic characteristics, oxidation, or color stability.
Key Words: Acyl-CoA desaturase • Fatty Acids • Linseed • Lipogenesis • Meat Quality • Pigs
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Introduction |
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-Linolenic acid (18:3n-3) is the precursor fatty acid for the synthesis of eicosapentaenoic acid (EPA; 20:5n-3) and docosahexaenoic acid (DHA; 22:6n-3), which play a major role in the control of cardiovascular diseases (Conquer and Holub, 1998
), and in neural and retinal development (Alessandri et al., 1998). As a result of these benefits, it is now widely recommended that the consumption of long-chain n-3 PUFA be increased in the human diet. Changing the pig’s diet provides an effective method of changing the fatty acid composition of pig fat depots, thereby modifying the human dietary fat intake from pork (Wood and Enser, 1997). In particular, the n-3 PUFA level can be increased in pork by feeding sources such as linseed, which contains about one-third oil, of which more than 50% is 18:3n-3 (Enser et al., 2000; Matthews et al., 2000).
Most of the studies undertaken on dietary manipulation of n-3 fatty acid concentrations in pig lipids have examined the effect of feeding different levels of appropriate oils to pigs (Cunnane et al., 1990; Enser et al., 2000; Wiseman et al., 2000). However, the time required for the incorporation of significant amounts of n-3 PUFA into tissues is poorly documented. Also not fully described is how incorporation of n-3 PUFA into lipids affects other mechanisms for fatty acid deposition, in particular the major synthetic enzymes. The aim of this study was to examine the time course of incorporation of n-3 PUFA from linseed into plasma and tissue lipids in comparison with a control, grain-based diet. Concurrently, the dietary effects of linseed on the lipogenic enzymes and on a major synthetic enzyme, stearoyl-CoA-desaturase (which generates monounsaturated fatty acids), were also studied. Because PUFA affect meat quality traits, such as shelf life and flavor, due to their propensity to oxidize, meat quality was also investigated.
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Materials and Methods |
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Animals and Diets
Forty-eight (Duroc x Landrace x Large White) gilts weighing about 40 kg (live weight) were used in this study. Pigs from 12 litters were allocated on the basis of litter and weight into three equal groups fed each of two diets: a control diet or a high-linseed diet containing 6% whole crushed linseed. Six groups of eight pigs were housed in typical indoor pens and had ad libitum access to food from a single bulk feeder in each pen with four feeding spaces. Both diets were pelleted and formulated to meet the requirements of the growing/finishing pig (Table 1). Both diets contained 20% CP and 1.20% lysine, and vitamin E was included in both diets at the level of 150 mg/kg. Fresh water was freely available via a nipple drinker in each pen. Animals were individually weighed each week and three groups of eight pigs from each diet were slaughtered at 20, 60, or 100 d after the beginning of the experiment.
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Carcass Evaluation and Sample Collection
Immediately after slaughter (30 min after stunning), samples of muscle and subcutaneous adipose tissue were excised from the last-rib region on the right side of each carcass, and were immediately assayed for enzyme activity (which began approximately 45 min after stunning). Additional muscle and fat samples were frozen and stored at -18°C for approximately 6 mo prior to lipid extraction/analysis and skatole quantification. Last-rib (P2) backfat thickness at a point 6.5 cm from the dorsal midline of each carcass was collected at approximately 45 min postslaughter using an optical probe by which the operator identified the boundary between subcutaneous fat and lean by viewing the tissues through an eyepiece (SFK HD, Hvidovore, Denmark).
Carcasses were held at ambient temperature (10 to 15°C) for 4 h before overnight chilling in a standard chiller at 1°C. About 24 h after slaughter, cold carcass weight and ultimate (24-h) pH of the longissimus muscle were recorded. Following removal of the head, feet, kidney, and leaf fat, left sides were fabricated into six anatomically defined primal cuts (belly, flank, foreloin, hindloin, leg, and shoulder) by the method described by Brown and Wood (1979). The foreloin (5th- to 13th-rib section) was removed during carcass fabrication and subsequently dissected into subcutaneous fat, intermuscular fat, lean, and bone.
Furthermore, a single 25-cm section of deboned longissimus lumborum was removed posterior to the last rib from the right sides of carcasses of pigs fed diets for 60 and 100 d (the pigs of typical commercial weights), vacuum-packaged, and aged for 10 d at 1°C. The conditioned section of muscle was then cut into three portions. One section was cut into two 1.27-cm-thick chops that were overwrapped with an oxygen-permeable, polyvinyl chloride film, and stored under simulated retail display conditions in a 4°C walk-in chill room under low-UV fluorescent light (750 lx illumination; 16 h on, 8 h off) for 7 d. The color of the lean was measured daily on one chop, and lipid oxidation in the muscle was measured on the other chop at the end of the 7-d display period. A 15-cm-long section was vacuum-packaged and stored at -20°C for approximately 2 mo before sensory analysis was conducted, and a 7.5-cm section was removed for objective measurement of meat tenderness.
Analyses
Plasma Analysis.
Plasma was separated by centrifugation at 2,000 x g for 15 min at 4°C, and then frozen at -20°C until further analyses. Total cholesterol was quantified using a commercial kit (Bio-Mérieux, Charbonnières-les-Bains, France) according to the method of Richmond (1973).
Fatty Acid Analysis.
Lipids were extracted from muscle and plasma by the chloroform:methanol procedure of Folch et al. (1957). The extracted lipids were separated on silicic acid columns (Jones Chromatography, Wales, U.K.) into neutral lipid and phospholipid fractions. Dietary lipids were extracted using diethyl ether (BSI, 1970), and adipose tissue was extracted using chloroform (Scollan et al., 2001). Fatty acid methyl esters from diets, adipose tissue, plasma, and muscle neutral lipid and phospholipid fractions were prepared using diazomethane and analyzed by GLC as described by Enser et al. (1998) with an internal standard (C21:0, Sigma, Gillingham, Dorset, U.K.) used to quantify fatty acids (g/100 g of total fatty acids).
Nutritional quality was described by the PUFA:saturated fatty acids (SFA) ratio expressed as: 18:2n-6 + 18:3n-3:14:0 + 16:0 + 18:0. Although we recognize that this is not an ideal indication of atherogenicity or thrombogenicity (Ulbricht and Southgate, 1991), it has been widely used. The n-6:n-3 ratio has been calculated as 18:2n-6:18:3n-3, which is relevant to the competition for synthesis of longer-chain PUFA. Because this ratio ignores the existence of longer-chain PUFA in the meat, the results were also expressed as 
n-6:n-3.
Enzyme Analysis.
The activity of stearoyl-CoA-desaturase was determined in muscle and subcutaneous adipose tissue homogenates obtained from the samples removed after slaughter. Weighed amounts of tissue (approximately 2 g) were homogenized (Polytron homogenizer; Bad Wilbad, Germany) in buffer containing 0.25 M sucrose and 0.05 M potassium, and centrifuged at 10,000 x g for 40 min at 4°C. Each incubation mixture for the measurement of stearoyl-CoA-desaturase contained an aliquot of supernatant, phosphate buffer, MgCl2, ATP, coenzyme A, NADH, and [14C]stearic acid, as described by Kouba et al. (1999). The activity was determined by measuring the conversion of [14C]stearic acid into [14C]oleic acid.
The activities of acetyl-CoA-carboxylase, malic enzyme, and glucose-6-phosphate-dehydrogenase were determined in muscle and subcutaneous adipose tissue. Weighed amounts of tissue were homogenized in 0.25 M sucrose buffer and centrifuged at 30,000 x g for 40 min at 4°C. The supernatant was assayed for malic enzyme, glucose-6-phosphate-dehydrogenase and acetyl-CoA-carboxylase, according to procedures outlined by Kouba et al. (1999), and NADH formation was measured at 37°C by absorbance at 340 nm. Acetyl-CoA-carboxylase was assayed in supernatants by the H14CO3-fixation method of Kouba et al. (1999).
Meat Analysis.
Objective muscle color was measured daily in chops subjected to 7 d of simulated display using a Minolta Chromameter II (Minolta U.K. Ltd., Milton Keynes, U.K.) calibrated daily against a standard white tile. The CIELAB L*, a*, and b* color space was used to determine color (McLarren, 1976); L* (darkness to lightness), a* (green to red color coordinate), and b* (blue to yellow coordinate) were recorded, and saturation index (a measure of the vividness or total color) was calculated from a* and b* values as (a*2 + b*2)1/2. Saturation index, or chroma, has been shown to be a good indicator of meat color changes during display (Hood and Riordan, 1973; Warris, 1996).
Thiobarbituric acid-reacting substances (TBARS) test was used to assess lipid oxidation in muscle after 7 d of simulated retail display according to the method of Tarlagdis et al. (1960). This method, based on distillation, measures malonaldehyde concentrations as a measure of rancidity and is reported as mg of malonaldehyde/kg of muscle. Vitamin E concentration in muscle was determined according to the method of Liu et al. (1996), except that single (not reverse) phase HPLC was used.
The muscle section for measurement of toughness was cooked in a water bath at 80°C to an internal temperature of 78°C, and was held in ice prior to cutting into 10 cubes (20 x 11 x 11 mm) with the long axis parallel to the muscle fiber direction. Cubes were sheared at right angles to the fibre direction using a Stevens CR Analyser (Mechtric Engineering Ltd, Benfleet, Essex, U.K.) equipped with a 50-kg load cell and fitted with Volodkevitch-type jaws. The first yield forces from the 10 cubes/muscle were averaged together for statistical analysis of shear force (Chrystall et al., 1994; Taylor et al., 1995).
Skatole was quantified in subcutaneous fat from each chop used for enzyme analysis by the method described by Annor-Frempong et al. (1997). Duplicate 10g samples were blended in 80 mL of distilled water brought to pH 10.5 with sodium hydroxide. Samples were transferred to round-bottomed flasks, and 1 µg of methylindole was added as an internal standard. The samples were heated to their boiling points and refluxed for 2 h using Likens-Nickerson condensers to trap the volatile components in pentane:ether (9:1), which were then quantified using GLC.
The 15-cm loin section designated for sensory analysis was thawed overnight at room temperature (10 to 15°C) and cut into 1.9-cm-thick chops. Chops were cooked on a "lincat" model GS7 griddle (Lincat, Lincoln, U.K.) set at 180°C. Chops were turned every 3 min until the internal temperature reached 80°C, as determined by a hand-held electronic probe employing a NiCr/NiAl type-K thermocouple (Comark, Welwyn Garden City, U.K.). Sensory assessments were performed using the Langford 10-female, trained taste panel, as described by Wiseman et al. (1999). After cooking, samples of lean and fat (2.0- to 2.5-cm cubes) were cut and presented to the panelists, and each of the eight sessions comprised samples from the three groups (control and linseed diets fed 60 or 100 d). Panelists rated chops on an eight-point scale for pork odor, abnormal odor, tenderness, juiciness, pork flavor, abnormal flavor, and overall liking (1 = extremely weak, extremely tough, extremely dry, extremely weak, and dislike extremely; 8 = extremely strong, extremely tender, extremely juicy, extremely strong, and like extremely).
Statistical Analysis
Differences between treatments were examined with two-way ANOVA using Genstat software (Genstat 5.3, Oxford, U.K.). The experimental unit was the individual pig, and the fixed effects included in the model were diet, time on feed (20, 60, and 100 d), and their interactions. For analysis of taste panel data, panelists’ scores for each chop were averaged, and ANOVA was performed with diet as the main effect and assessors and taste panel session as block effects, included in the statistical model. When a significant (P < 0.05) treatment effect was observed, Bonferroni’s multiple comparison test was performed.
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Results |
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Diet had no effect (P > 0.05) on animal growth, any carcass characteristic, or foreloin composition (Tables 2 and 3); however, P2 fat thickness increased (P < 0.001) with time on feed. Additionally, proportions of subcutaneous fat and intermuscular fat, as well as the lean:bone ratio, increased (P < 0.01), and the proportions of bone and lean and the lean:total fat ratio decreased (P < 0.01) as time on feed increased from 20 to 100 d.
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The muscle phospholipid proportion decreased (P < 0.05) with time in both diets; however, the neutral lipid content increased (P < 0.001) with time (Table 4). The total lipid content of muscle increased between 20 and 60 d for pigs fed the control diet (P < 0.01), and between 60 and 100 d for pigs fed the linseed diet (P < 0.01). The backfat lipid content increased between 20 and 60 d (P < 0.01), but then remained almost constant (P > 0.05) in both diets. Pigs fed the linseed diet had lower (P < 0.05) concentrations of neutral lipid and total lipid in muscle of pigs fed for 60 d; however, there was no (P > 0.05) effect of diet on total lipid content of backfat or on phospholipid content of muscle.
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Muscle Fatty Acids.
Total PUFA (g/100 g fatty acids) declined (P < 0.01) with time on feed, and total SFA increased (P < 0.01) in muscle, regardless of diet (Table 5). The percentage of 18:2n-6 decreased (P < 0.001) with time, whereas the percentage of 18:3n-3 decreased (P < 0.05) between 60 and 100 d in pigs fed the linseed diet, and decreased (P < 0.001) throughout the experiment in pigs fed the control diet. Percentages of EPA, docosapentaenoic acid (DPA), and DHA decreased (P < 0.01) with time on feed, regardless of diet.
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Muscle Neutral Lipids and Phospholipids.
The effect of time on feed on fatty acid composition of neutral lipids was quite similar to the effects on muscle total fatty acids (Table 6). However, proportions of PUFA, SFA, and 18:2n-6 in phospholipids did not change (P > 0.05) with time (Table 7).
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Adipose Tissue Fatty Acids.
Similar to that observed in muscle tissue, total PUFA and 18:2n-6 proportions decreased with time (P < 0.001), whereas the concentration of SFA increased (P < 0.01) with time on feed, regardless of diet (Table 8). However, the percentage of DPA remained constant across all slaughter times in pigs fed the linseed diet.
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Plasma Fatty Acids and Cholesterol.
Plasma fatty acids are known to respond rapidly to dietary changes. Plasma was characterized by a higher (P < 0.001) percentage of PUFA and a lower (P < 0.001) percentage of SFA and MUFA for both diets compared with adipose tissue and muscle (Table 9). The linseed diet led to an increase (P < 0.01) in the proportion of n-3 PUFA; however, the proportion of DHA was lower (P < 0.01) in pigs fed the linseed diet than the control diet. The percentage of 18:2n-6 was very high for both diets compared with adipose tissue and muscle, and total plasma fatty acid concentration was highest (P < 0.01) after 60 d on feed, regardless of diet. Compared with the control diet, feeding crushed linseed resulted in a higher (P < 0.01) fatty acid concentration in pigs slaughtered at 20 d, and lower (P < 0.05) concentration in pigs slaughtered at 60 d; concentrations were similar (P > 0.05) after 100 d on feed. The cholesterol concentration in plasma showed no clear pattern with regard to diet or time on feed.
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. Although TBARS values were low (<0.2 mg of malonaldehyde/kg), pork from pigs fed the linseed diet had higher (P < 0.001) TBARS values than pork from pigs fed the control diet. Time on feed had no (P > 0.05) effect on measures of lipid oxidation or cooked meat tenderness; however, pork from linseed-fed pigs was tougher (P < 0.05) than pork from pigs fed the control diet.
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Saturation values (purity of red colour) decreased (P < 0.05) over the 7-d display period, reflecting the change from red to brown commonly observed in displayed meat (Hood and Riordan, 1973). Results were quite similar for the two diets, and there was no (P > 0.05) effect of time on feed or diet (results not shown).
Skatole.
Skatole concentration increased (P < 0.01) with time on feed in pigs fed the control diet, whereas there was no effect (P > 0.05) of time on feed on skatole levels in pigs fed the linseed diet (Figure 1). Skatole level was influenced by dietary treatment, with pigs fed linseed having lower (P < 0.001) levels of skatole in backfat than pigs fed the control diet.
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. There was no effect (P > 0.05) of days on feed on any of the sensory attributes. However, pork from pigs fed the linseed diet had lower (P < 0.05) pork odor in fat, higher (P < 0.05) abnormal odor in the fat, and lower (P < 0.05) lean flavor-liking scores than pork from pigs fed the control diet.
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The stearoyl-CoA-desaturase activity in backfat increased (P < 0.001) between 20 and 60 d in pigs fed both diets, and then decreased (P < 0.001) between 60 and 100 d in pigs fed the control diet, whereas the activity remained similar (P > 0.05) between 60 and 100 d in pigs fed the linseed diet (Table 12). There was no effect (P > 0.05) of time on feed on stearoyl-CoA-desaturase activity in muscle. The acetyl-CoA-carboxylase activity decreased (P < 0.001) between 20 and 60 d in backfat of pigs fed either diets, and between 20 and 60 d in muscle (P < 0.05) of pigs fed the control diet. There was no effect (P > 0.05) of time on feed on malic enzyme activity in the adipose tissue, whereas activity was increased (P < 0.01) in muscle. Furthermore, time on feed did not (P > 0.05) affect glucose-6-phosphate-dehydrogenase activity in muscle, but did decrease (P < 0.01) its activity in adipose tissue.
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Discussion |
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, Warnants et al. (1999), and Riley et al. (2000) drew similar conclusions.
The results are in general agreement with other studies showing that 18:3n-3 and 20:5n-3 are increased when the level of linseed increases in the diet (Enser et al., 2000; Matthews et al., 2000; Riley et al., 2000). The actual changes observed differ between studies according to the amount of linseed in the diet, time on feed, and the ratio of 18:3n-3 to 18:2n-6 because these compete for inclusion into tissue lipids and for the enzymes responsible for desaturation and elongation (Specht-Overholt et al., 1997). Furthermore, rapid changes in 18:3n-3 and 20:5n-3 concentrations in the muscle of pigs fed linseed-fortified diets have also been observed by Fontanillas et al. (1998) and Riley et al. (2000). For example, Riley et al. (2000) suggested that ratios in muscle total fatty acids were of 3.5 for 18:3n-3 and 2.5 for 20:5n-3 between a high-linseed (114g/kg of whole linseed) diet fed for 24 d and a control diet. Cameron et al. (2000) found ratios of 2.4 for 18:3n-3 and 2.3 for 20:5n-3 in plasma total lipids after only 4 d in pigs fed a diet containing 80g/kg whole linseed. Although 20:5n-3 and 22:5n-3 concentrations were increased by feeding the linseed diet, that of 22:6n-3 was not affected in the present study. This block on DHA production from 18:3n-3 has also been observed in other published work (Riley et al., 2000).
Concerns about excess SFA and a deficiency of n-3 PUFA in the human diet have led to recommendations that the ratio of PUFA:SFA be increased by 0.4 or higher, and that the ratio of n-6:n-3 fatty acids in the diet be lowered to between 1 and 4 (HMSO, 1984; HMSO, 1994). Feeding pigs the linseed diet produced a PUFA:SFA ratio in muscle of 0.54 and 0.38 in the 60- and 100-d groups, respectively, and a PUFA:SFA ratio in adipose tissue of 0.67 and 0.48, respectively. All of these ratios are equal to or higher than 0.4. Furthermore, feeding crushed linseed caused a large decrease in the n-6:n-3 ratios in muscle (3.00 vs. 7.34 and 3.11 vs. 8.71, respectively, for pigs fed 60 and 100 d) and adipose tissue (2.05 vs. 6.30 and 2.07 vs. 6.39, respectively, for pigs fed 60 and 100 d). The effects of linseed diet on these ratios are in accordance with results of Riley et al. (2000), who found the same ratios in muscle (3.9 with a 3% linseed diet vs. 8.5 with a control diet) and adipose tissue (3.2 with a 3% linseed diet vs. 8.4 with a control diet), and Matthews et al. (2000), who reported n-6:n-3 in muscle of 3.5 with a 5% linseed diet compared to 7.2 with a control diet.
Assuming the average annual U.K. pork consumption of 22.2 kg with a lean:fat ratio of 10:1, pork from pigs fed the linseed diet for 60 d would contribute approximately 114 g of 18:3n-3 and 9.8 g of C20 to C22n-3 PUFA to the diet. This intake of 18:3n-3 is about 20% of that found to reduce the risk of arrhythmia in American women (Hu et al., 1999). There is increasing evidence to suggest that 18:3n-3 itself has health benefits apart from acting as a precursor to EPA and DHA (Williams, 2000). For C20 to C22n-3 PUFA, the intake of 9.8 g is about 13.5% of the 73 g recommended by the HMSO (1994). These levels of n-3 PUFA in pork would make an important contribution to a healthier diet.
Stearoyl-CoA-desaturase generates MUFA from SFA (Bloomfield and Bloch, 1960; Marsh and James, 1962; Gelhorn and Benjamin, 1965). The 40% decrease in the stearoyl-CoA-desaturase activity in the backfat of pigs fed crushed linseed for 60 d compared with those fed the control diet resulted in a obvious reduction in the MUFA percentage, which is consistent with previous studies (Romans et al., 1995; Specht-Overholt et al., 1997; Matthews et al., 2000). Results of the present study showed that the changes in the MUFA percentage could be attributed, at least in part, to a reduction in stearoyl-CoA-desaturase activity. After 60 d of feeding crushed linseed, the incorporation of n-3 PUFA was also greatest in backfat. The observation that linolenic acid inhibited stearoyl-CoA-desaturase activity in pig adipose tissue supports previous research from our laboratory indicating that dietary linoleic acid had an inhibitory effect on stearoyl-CoA-desaturase activity in swine (Kouba and Mourot, 1998).
Acetyl-CoA-carboxylase activity catalyzes the first step in the fatty acid biosynthetic process. This enzyme has a key role in the regulation of fatty acid biosynthesis in animal tissues and is generally considered to be a rate-limiting enzyme of lipogenesis in animals (Numa et al., 1970), especially in pigs (Mersmann et al., 1973; Scott et al., 1981). Malic enzyme and glucose-6-phosphate-dehydrogenase are the main enzymes involved in supplying NADPH for the reductive biosynthesis of fatty acids (Wise and Ball, 1964; Young et al., 1964). Results of the present study showed no effect of feeding crushed linseed with a high of n-3 PUFA content on these enzyme activities, which is in contrast to previous results from our laboratory where activities of these enzymes were actually increased by dietary linoleic acid in pigs (Kouba and Mourot, 1998). In this previous study, the diets (control and experimental) were isolipidic, whereas in the present study, the fat content of the linseed diet was twice that of the control diet. Several studies have shown that when the PUFA level increased in the diet due to increase in the dietary fat content, the lipogenic enzyme activities were similar in both experimental and control diets (Mersmann et al., 1976; Busboom et al., 1991).
In the longissimus muscle, vitamin E was lower in pigs fed the linseed diet for 60 d than in those fed the control diet, whereas there was no effect of the diet in any other slaughter group. It was also in pigs fed for 60 d that the difference between the PUFA percentages achieved with the two diets was at its highest in muscle (13.8 vs. 19.2% for control and linseed diets, respectively). This concurs with the observations of others who have reported lower levels of vitamin E in porcine tissues containing high PUFA levels (Meydani et al., 1987; Wang et al., 1996; Leskanich et al., 1997).
The slightly lower oxidative stability of the muscle from pigs fed crushed linseed diet compared to pigs fed the control diet was probably due to the higher content of PUFA in those animals. Measures of oxidative rancidity (TBARS values) were low (<0.2 mg of malonaldehyde/kg), indicating that there was no rancidity problem in pork from pigs fed the linseed diet. Consumers are unlikely to detect off-flavors at values below a threshold of about 0.5 mg of malonaldehyde/kg (Gray and Pearson, 1987). However, Shackelford et al. (1990) demonstrated that trained taste panelists could actually detect off-flavors in cooked hams that contained 3% 18:3n-3 muscle lipid (a level similar to that found in muscle of pigs fed the linseed diet). Results from the present study indicated that there was a tendency for lower odor and flavor attributes in the pigs fed linseed. Even though differences were small, pork from pigs fed crushed linseed had a lower pork odor, higher abnormal odor (in fat), and a lower flavor liking score. Other workers found no major difference in sensory panel evaluations of pork from pigs fed a high-linseed diet (Ahn et al., 1996; Oeckel et al., 1996; Matthews et al., 2000).
An increased concentration of skatole in fat is a major reason for boar taint (Babol and Squires, 1995). The skatole concentrations found in the current trial were similar to those obtained in gilts by Wiseman et al. (1999), and were much lower than the skatole concentration of 0.25 mg/kg of fat, which leads to sensory problems in cooked meat (Mortensen and Sorensen, 1984; Mortensen et al., 1986; Claus et al., 1994). Feeding the linseed diet led to a much lower skatole concentration, and this could be a response to the higher NDF and ADF content of the linseed diet, causing modification of hindgut fermentation patterns (Wiseman et al., 1999). Another possibility arises from the work of Jeong and Yun (1995), who demonstrated that myristicin (a benzodioxole compound found in linseed) induces hepatic cytochrome P450 enzymes. As skatole is metabolized in pig liver to different metabolites by cytochrome P4502E1 (Squires and Lundström, 1997; Doran et al., 2002), myristicin could decrease skatole levels as a consequence of the induction of hepatic cytochrome P4502E1 enzymes.
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Footnotes |
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2 Correspondence—phone: 02-23-48-53-67; fax: 02-23-48-59-00; E-mail: kouba{at}st-gilles.rennes.inra.fr.
Received for publication April 5, 2002. Accepted for publication March 31, 2003.
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-tocopherol status of C57BL/6Nia mice. Lipids 22:345–350.[Medline]
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S. T. Larsen, B. R. Wiegand, F. C. Parrish Jr., J. E. Swan, and J. C. Sparks Dietary conjugated linoleic acid changes belly and bacon quality from pigs fed varied lipid sources J Anim Sci, January 1, 2009; 87(1): 285 - 295. [Abstract] [Full Text] [PDF]
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J. K. Apple, C. V. Maxwell, B. R. Kutz, L. K. Rakes, J. T. Sawyer, Z. B. Johnson, T. A. Armstrong, S. N. Carr, and P. D. Matzat Interactive effect of ractopamine and dietary fat source on pork quality characteristics of fresh pork chops during simulated retail display J Anim Sci, October 1, 2008; 86(10): 2711 - 2722. [Abstract] [Full Text] [PDF]
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 V. Razmaite, S. Kerziene, and A. Siukscius Pork Fat Composition of Male Hybrids from Lithuanian Indigenous Wattle Pigs and Wild Boar Intercross Food Science and Technology International, June 1, 2008; 14(3): 251 - 257. [Abstract] [PDF]
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M. A. Gorocica-Buenfil, F. L. Fluharty, C. K. Reynolds, and S. C. Loerch Effect of dietary vitamin A concentration and roasted soybean inclusion on marbling, adipose cellularity, and fatty acid composition of beef J Anim Sci, September 1, 2007; 85(9): 2230 - 2242. [Abstract] [Full Text] [PDF]
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C. Farmer, H. V. Petit, H. Weiler, and A. V. Capuco Effects of dietary supplementation with flax during prepuberty on fatty acid profile, mammogenesis, and bone resorption in gilts J Anim Sci, July 1, 2007; 85(7): 1675 - 1686. [Abstract] [Full Text] [PDF]
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S. Zhang, T. J. Knight, K. J. Stalder, R. N. Goodwin, S. M. Lonergan, and D. C. Beitz Effects of breed, sex, and halothane genotype on fatty acid composition of pork longissimus muscle J Anim Sci, March 1, 2007; 85(3): 583 - 591. [Abstract] [Full Text] [PDF]
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