Relationship between the expression of hepatic but not testicular 3b-hydroxysteroid dehydrogenase with androstenone deposition in pig adipose tissue
Nicolau-Solano, S. I. print, McGivan, J. D. print, Whittington, F. M. print, Nieuwhof, G. J. print, Wood , J. D. print and Doran (nee Udovikova), O. print (2006) Relationship between the expression of hepatic but not testicular 3b-hydroxysteroid dehydrogenase with androstenone deposition in pig adipose tissue. Journal of Animal Science, 84 (10). pp. 2809-2817. ISSN 0021-8812
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Publisher's URL: http://dx.doi.org/10.2527/jas.2005-595
ABSTRACT: This study investigated the relationship between expression of hepatic and testicular 3β- hydroxysteroid dehydrogenase (3β-HSD) and accumulation of androstenone in adipose tissue because of its relation to boar taint. The experiments were performed on 13 Large White (50%) × Landrace (50%) and Meishan (25%) × Large White (25%) × 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 3β-androstenol. In this study, the formation of 3β-androstenol was inhibited by the specific 3β-HSD inhibitor trilostane. These results are the first direct confirmation that 3β-HSD is the enzyme responsible for androstenone metabolism in the pig. The expression of the hepatic but not testicular 3β-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 3β-HSD pro-tein in the liver of high androstenone pigs was also accompanied by a reduced level of 3β-HSD mRNA (P < 0.001), which suggests a defective regulation of the hepatic 3β-HSD expression at the level of transcription. In contrast, expression of the testicular 3β-HSD protein did not differ between animals with high and low androstenone levels (P > 0.05) and was lower compared with the hepatic 3β-HSD expression. Cloning and sequencing of the 3β-HSD coding regions established that the hepatic and testicular 3β-HSD cDNA have identical sequences, which were 98% similar to the human 3β- HSDisoform I. It is suggested that expression of a single 3β-HSD gene is regulated by different mechanisms in pig liver and testis. The liver-specific regulation of 3β- 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.
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