Relationship between the expression of hepatic but not testicular 3β-hydroxysteroid dehydrogenase with androstenone deposition in pig adipose tissued

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(2) = 0.64; P < 0.001) and was accompanied by a reduced rate of the hepatic kandrostenone 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.