Relationship between the expression of hepatic but not testicular 3β-hydroxysteroid dehydrogenase with androstenone deposition in pig adipose tissue1

Abstract

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.

Genetic and metabolic aspects of androstenone and skatole deposition in pig adipose tissue: A review(Open Access publication)

“…The expression of 3β-HSD protein, which is lower in liver microsomes from Meishan pigs (exhibiting high levels of androstenone) than from Large White pigs (exhibiting low levels of androstenone in fat), is accompanied by a reduced level of the corresponding mRNA [29]. This result suggests a defective regulation of the hepatic 3β-HSD expression at the transcription level [29]. Although 3β-HSD is active in both liver and testis, only expression of the hepatic form is negatively correlated with androstenone levels in fat [29].…”

“…In pig, a single gene HSD3B, encodes this enzyme (Tab. I) and its expression is regulated by a tissue-specific mechanism [29]. This gene is expected to be localized between 90 and 100 cM on the linkage map of SSC4, near the region where a QTL has been detected for androstenone level in fat (105 cM by Lee et al [21]).…”

“…This result suggests a defective regulation of the hepatic 3β-HSD expression at the transcription level [29]. Although 3β-HSD is active in both liver and testis, only expression of the hepatic form is negatively correlated with androstenone levels in fat [29]. In pig, a single gene HSD3B, encodes this enzyme (Tab.…”

Relationship between carcass weight, adipose tissue androstenone level and expression of the hepatic 3β-hydroxysteroid dehydrogenase in entire commercial pigs

“…The optimum Nicolau-Solano, Whittington, Wood and Doran amount of protein required for the analysis has been determined in our previous work and was 6 mg per well (Nicolau-Solano et al, 2006). The microsomal proteins were separated by SDS-PAGE, electroblotted onto a nitrocellulose membrane, pore size 0.45 mm (Bio-Rad, Hertfordshire, UK) at a constant voltage of 100 V for 1 h and probed with rabbit anti-porcine 3b-HSD antibody for 1.5 h. The antibody was produced against a synthetic peptide corresponding to amino acids 357 to 370 of the porcine 3b-HSD protein (GenBank accession no.…”

“…The reason for the high androstenone accumulation in some pigs is not clear. Excessive androstenone levels can be attributed, at least partially, to defective expression and activity of the hepatic androstenone-metabolising enzyme 3b-hydroxysteroid dehydrogenase (3b-HSD) Nicolau-Solano et al, 2006). The mechanism regulating 3b-HSD expression in pig liver remains unknown.…”