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The objectives of this study were 1) to determine whether selection toward less subcutaneous fat thickness at constant intramuscular fat content in pigs is related to tissue-specific changes in the expression of lipogenic enzymes acetyl-CoA carboxylase (ACC), stearoyl-CoA desaturase (SCD), and A% desaturase ([DELTA]6d); and 2) to investigate tissue specific distribution of the porcine ACC, SCD, and [DELTA]6d. The study was conducted on 20 purebred Duroc barrows. Ten animals were from a group selected for decreased subcutaneous fat thickness at constant intramuscular fat content (experimental group). The other 10 animals were from the unselected (control) group. Distribution of ACC, SCD, and [DELTA]6d was investigated in semimembranosus muscle (SM), subcutaneous adipose tissue (SA), liver (L), kidney (K), heart (H), diaphragm (D), rectus capitis muscle (RCM), and abdominal fat (AF). The enzyme expression was studied in 10 animals in the case of SM and SA and in 4 animals in the case of other tissues. The following expression pattern was established for ACC: SM [less than or equal to] H = K [less than or equal to] D< RCM < L < AF = SA, whereas the expression patterns for SCD and [DELTA]6d proteins were SM < H < RCM < D < L < K < AF = SA and RCM = SM = D < L [less than or equal to] H < SA < K < AF, respectively. Expression of ACC and SCD proteins was less in subcutaneous adipose tissue of the experimental animals when compared with the control group (P < 0.001). However, no difference (P > 0.1) in ACC and SCD protein expression between the control and experimental groups was observed in SM. Expression of [DELTA]6d protein did not differ between the control and experimental groups for SA (P = 0.47) or SM (P = 0.31). There was a positive relationship between muscle SCD protein expression and intramuscular fat content (r = 0.48, P < 0.05). Intramuscular fat content did not correlate with ACC or [DELTA]6d protein expression (P = 0.23 and P = 0.80, respectively). We conclude that SCD might be an effective potential biomarker for intramuscular fat deposition. Key words: intramuscular fat, lipogenic enzyme expression, meat quality, pig, subcutaneous fat doi: 10.2527/jas.2009-2091

An excessive accumulation of androstenone in pig adipose tissue is a major contributor to the phenomenon of boar taint. Androstenone deposition is dependent on the rate of androstenone biosynthesis in testis and androstenone degradation in liver. The aim of the current study was to examine the possibility of the existence of breed-specific mechanisms controlling androstenone accumulation in pig adipose tissue. The specific objective was to investigate the expression of some of the key enzymes involved in testicular and hepatic androstenone metabolism in pigs of 2 breeds by using animals with high and low androstenone concentrations within each breed. The study was conducted with Norwegian Landrace (N. Landrace) and Duroc boars. The mean androstenone values for the low- and high-androstenone groups were 0.1 [+ or -] 0.01 [micro]g/g and 7.58 [+ or -] 0.68 [micro]g/g for N. Landrace boars, and 0.22 [+ or -] 0.04 [micro]g/ g and 13.55 [+ or -] 1.14 [micro]g/g for Duroc boars. The enzymes investigated were 3[beta]-hydroxysteroid dehydrogenase (3[beta]-HSD), cytochrome P450-c17, and sulfotransferase 2B1 (SULT2B1). Expression of cytochrome P450-c17 in liver and testis did not differ between animals with high and low androstenone concentrations in either the N. Landrace or Duroc breed. Expression of hepatic 3[beta]-HSD, which catalyzes the first stage of androstenone degradation, was decreased in high-androstenone N. Landrace boars (P < 0.01), but not in high-androstenone Duroc boars. In contrast, the expression of hepatic SULT2B1, which catalyzes the second stage of steroid catabolism, was decreased in high-androstenone Duroc animals (P < 0.05), but not in high-androstenone N. Landrace animals. Sulfotransferase 2B1 was also inhibited in testis of high-androstenone pigs of both breeds compared with low-androstenone animals. We report breed differences in expression of the androstenone-metabolizing enzymes 3[beta]-HSD and SULT2B1 in the liver of high- and low-androstenone pigs. It is suggested that accumulation of androstenone in adipose tissue of N. Landrace boars might be related to a low rate of hepatic androstenone degradation in metabolic stage I, whereas the high androstenone concentration in Duroc boars might be related to a low rate of androstenone metabolism in metabolic stage II. Key words: androstenone, breed, cytochrome P450-c17, 3[beta]-hydroxysteroid dehydrogenase, pig, sulfotransferase 2B1

The entire sequence of the pig 3 [beta]-hydroxysteroid dehydrogenase (3 [beta]-HSD) gene has recently become known. This gene is deemed to be important in androstenone metabolism in pig liver, and its defective expression has been shown to be related to androstenone accumulation in adipose tissue and the development of boar taint. The aim of the present work was to do the following: 1) define the structure of the pig 3 [beta]-HSD gene and 2) compare 3 [beta]-HSD DNA sequences from pigs of different breeds, which vary in adipose tissue androstenone levels, with the purpose of identifying a polymorphism that might be responsible for differential 3 [beta]-HSD expression. The 5' flanking and the coding region of 3 [beta]-HSD were cloned and sequenced by conventional techniques. The 3 [beta]-HSD coding regions were identical in pigs of different breeds and in animals with high and low androstenone levels. Significant sequence variations were found in the 5' flanking region of the 3 [beta]-HSD gene, where differences in the number of TTAT repeats and 3 SNP were observed. The SNP were associated with the number of the TTAT repeats. These variations in the DNA sequence of the 3 [beta]-HSD gene were not associated with the androstenone level in s.c. adipose tissue but were breed-dependent. The results of this work might be used for detection of the presence of Meishan genes in Western pig breeds, especially if the phenotype is not clearly established. Key words: breed, 3 [beta]-hydroxysteroid dehydrogenase, gene, pig, polymorphism

This study investigated the relationship between expression of hepatic and testicular 3 [beta]-hydroxysteroid dehydrogenase (3 [beta]-HSD) and accumulation of androstenone in adipose tissue because of its relation to boar taint. The experiments were performed on 13 Large White (50%) x Landrace (50%) and Meishan (25%) x Large White (25%) x Landrace (50%), pigs, which differed in the level of backfat androstenone. Our previous work showed that the major product of the hepatic androstenone metabolism is 3 [beta]-androstenol. In this study, the formation of 3 [beta]-androstenol was inhibited by the specific 3 [beta]-HSD inhibitor trilostane. These results are the first direct confirmation that 3 [beta]-HSD is the enzyme responsible for androstenone metabolism in the pig. The expression of the hepatic but not testicular 3 [beta]-HSD protein showed a negative relationship with the level of backfat androstenone ([r.sup.2] = 0.64; P < 0.001) and was accompanied by a reduced rate of the hepatic androstenone clearance. Low expression of 3 [beta]-HSD protein in the liver of high androstenone pigs was also accompanied by a reduced level of 3 [beta]-HSD mRNA (P < 0.001), which suggests a defective regulation of the hepatic 3 [beta]-HSD expression at the level of transcription. In contrast, expression of the testicular 3 [beta]-HSD protein did not differ between animals with high and low androstenone levels (P > 0.05) and was lower compared with the hepatic 3 [beta]-HSD expression. Cloning and sequencing of the 3 [beta]-HSD coding regions established that the hepatic and testicular 3 [beta]-HSD cDNA have identical sequences, which were 98% similar to the human 3 [beta]-HSD isoform I. It is suggested that expression of a single 3 [beta]-HSD gene is regulated by different mechanisms in pig liver and testis. The liver-specific regulation of 3 [beta]-HSD expression contributes to the low rate of hepatic androstenone metabolism and therefore can be considered as one of the factors regulating deposition of androstenone in pig adipose tissue and subsequent development of boar taint. Key words: androstenone, boar taint, 3 [beta]-hydroxysteroid dehydrogenase, pig

The experiment was conducted to test the hypothesis that the replacement of cereal with low-starch feed ingredients in lambs' finishing diets supplemented with oils could prevent the accumulation of -10-18:1 in meat. Forty lambs were fed 1 of 4 diets supplemented with soybean oil (5.9%) and fish oil (1%) for 6 wk before slaughter. The control (CON) diet contained 43% barley, and in the other diets, barley was completely replaced by dehydrated citrus pulp (DCP), dehydrated sugar beet pulp (DBP), or soybean hulls (SH). Growth performance, feed intake, and carcass and meat quality traits were analyzed. At slaughter, LM samples were collected for gene expression evaluation, and 3 d after slaughter, LM and subcutaneous (s.c.) fat samples were collected for fatty acid analysis. None of the diets affected meat quality, but the DCP diet reduced ADG ( < 0.05) and the DCP and SH diets decreased the feed-to-gain ratio ( < 0.01). The DCP diet increased ( < 0.05) the risk of parakeratosis and the severity of the lesions. Moreover, the DBP treatment led to increased a* (redness) and b* (yellowness) in s.c. fat compared with the CON treatment ( < 0.05). The lipid content of LM did not differ ( > 0.05) with treatment and averaged 34.4 g/kg of meat. Diets had no effect ( > 0.05) on SFA, PUFA, and -MUFA sums and on the -6:-3 ratio in both LM and s.c. fat. A lower expression of fatty acid synthase (FASN) was found with the DCP treatment than with the other treatments ( < 0.001). All treatments showed a high accumulation of -10-18:1, averaging 91 mg/g fatty acid in LM and 147 mg/g fatty acid in s.c. fat. The concentration of -11-18:1 in the tissues was considerably lower than that of -10-18:1, and thus the -10-18:1:-11-18:1 ratio was above 3 with all treatments. Despite this, the SH diet clearly promoted a larger deposition of -11-18:1 and -9,-11-18:2 in tissues compared with the other treatments. () gene expression and SCD activity index in LM were reduced with the SH diet compared with the CON and DCP diets. Overall, these results clearly showed, for the first time, that low-starch/high-NDF diets are not able to prevent the establishment of -10 shifted rumen biohydrogenation pathways, evaluated by the deposition of biohydrogenation intermediates in lamb meat and fat.

The aims of the study were 1) to investigate effects of a low protein diet on fatty acids content and composition of the LM and subcutaneous adipose tissue in 3 genetically diverse breeds, Large White × Landrace, Alentejano, and Bizaro, and 2) to determine whether the effect of the low protein diet of fatty acid composition is associated with dietary modulation of stearoyl-CoA desaturase (SCD) protein expression. The experiments were conducted on 12 Large White × Landrace, 12 Alentejano, and 10 Bízaro female and male pigs. The average animal BW at the beginning of experiments was 40.8, 40.7, and 38.3 kg for Large White × Landrace, Alentejano, and Bízaro, respectively, and the BW of animals at slaughter was 90 kg. The diets contained 202 or 169 g/kg DM of CP (high and low protein diets, respectively) and were balanced in essential AA. The diets were fed until the animals reached 90 kg BW (approximately 73 d). It was established that Large White × Landrace pigs had a less (P = 0.001) total fatty acid content in subcutaneous adipose tissue when compared with Alentejano and Bízaro and less (P < 0.001) intramuscular fat (IMF) content when compared with Alentejano. There was a positive relationship between SCD protein expression in the LM and MUFA content (r = 0.627, P = 0.029) and SCD protein expression and total muscle fatty acids content (r = 0.725, P = 0.008) in Large White × Landrace but not in Alentejano and Bizaro breeds. It has been suggested that SCD protein expression is associated with regulation of fat deposition only in breeds with genetic predisposition to a low IMF content.

Objectives of this study were to compare fatty acid composition of subcutaneous adipose tissue of entire boars, barrows, and male pigs vaccinated against boar taint with a vaccine containing a GnRH analogue-protein conjugate (Improvac, Pfizer Animal Health) and to investigate the association between fatty acid composition and protein expression of key lipogenic enzymes in entire boars, barrows, and vaccinated pigs. Differences between groups were observed in the content of total SFA (P≤0.001), MUFA (P=0.035), and n-6 PUFA (P≤0.001) but not n-3 PUFA (P=0.373). Total SFA were greater (P<0.001) in barrows and vaccinated pigs compared with entire animals. This was accompanied by an increase (P<0.05) in the protein expression of the lipogenic enzyme fatty acid synthase in barrows and vaccinated pigs. Total MUFA content was increased (P<0.001) in barrows compared with entire and vaccinated pigs. This was not accompanied (P>0.05) by an increase in expression of stearoyl-CoA desaturase protein, the enzyme catalyzing MUFA biosyntheses. Total n-6 PUFA content did not differ (P<0.001) between entire and vaccinated pigs but was lower in barrows. Expression of Δ6-desaturase protein, one of the key enzymes of PUFA biosynthesis, was greater (P<0.05) in vaccinated pigs than in barrows but did not differ significantly between vaccinated and entire animals. We conclude that fatty acid profile of animals vaccinated against boar taint is similar to that of entire male pigs and that the effect of physical castration and vaccination on fatty acid composition involves changes in lipogenic enzyme protein expression.

This study investigated the relationship between expression of hepatic and testicular 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and accumulation of androstenone in adipose tissue because of its relation to boar taint. The experiments were performed on 13 Large White (50%) x Landrace (50%) and Meishan (25%) x Large White (25%) x Landrace (50%), pigs, which differed in the level of backfat androstenone. Our previous work showed that the major product of the hepatic androstenone metabolism is 3beta-androstenol. In this study, the formation of 3beta-androstenol was inhibited by the specific 3beta-HSD inhibitor trilostane. These results are the first direct confirmation that 3beta-HSD is the enzyme responsible for androstenone metabolism in the pig. The expression of the hepatic but not testicular 3beta-HSD protein showed a negative relationship with the level of backfat androstenone (r2 = 0.64; P < 0.001) and was accompanied by a reduced rate of the hepatic androstenone clearance. Low expression of 3beta-HSD protein in the liver of high androstenone pigs was also accompanied by a reduced level of 3beta-HSD mRNA (P < 0.001), which suggests a defective regulation of the hepatic 3beta-HSD expression at the level of transcription. In contrast, expression of the testicular 3beta-HSD protein did not differ between animals with high and low androstenone levels (P > 0.05) and was lower compared with the hepatic 3beta-HSD expression. Cloning and sequencing of the 3beta-HSD coding regions established that the hepatic and testicular 3beta-HSD cDNA have identical sequences, which were 98% similar to the human 3beta-HSD isoform I. It is suggested that expression of a single 3beta-HSD gene is regulated by different mechanisms in pig liver and testis. The liver-specific regulation of 3beta-HSD expression contributes to the low rate of hepatic androstenone metabolism and therefore can be considered as one of the factors regulating deposition of androstenone in pig adipose tissue and subsequent development of boar taint.