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

October 4, 2006 — S. I. Nicolau-Solano, J. D. McGivan, F. M. Whittington, G. J. Nieuwhof, J. D. Wood and O. Doran

This study investigated the relationship between expression of hepatic and testicular 3ß-hydroxysteroid dehydrogenase (3ß-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 3ß-androstenol. In this study, the formation of 3ß-androstenol was inhibited by the specific 3ß-HSD inhibitor trilostane. These results are the first direct confirmation that 3ß-HSD is the enzyme responsible for androstenone metabolism in the pig. The expression of the hepatic but not testicular 3ß-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 3ß-HSD protein in the liver of high androstenone pigs was also accompanied by a reduced level of 3ß-HSD mRNA (P < 0.001), which suggests a defective regulation of the hepatic 3ß-HSD expression at the level of transcription.

In contrast, expression of the testicular 3ß-HSD protein did not differ between animals with high and low androstenone levels (P > 0.05) and was lower compared with the hepatic 3ß-HSD expression. Cloning and sequencing of the 3ß-HSD coding regions established that the hepatic and testicular 3ß-HSD cDNA have identical sequences, which were 98% similar to the human 3ß-HSD isoform I.

It is suggested that expression of a single 3ß-HSD gene is regulated by different mechanisms in pig liver and testis. The liver-specific regulation of 3ß-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.

J. Anim. Sci. 2006. 84:2809-2817
© 2006 American Society of Animal Science

S. I. Nicolau-Solano, J. D. McGivan, F. M. Whittington, G. J. Nieuwhof, J. D. Wood and O. Doran Department of Clinical Veterinary Science, University of Bristol, Langford, Bristol, BS40 5DU, UK (SIN, JDM, FMW,JDW, OD); Meat and Livestock Commission, PO Box 44, Winterhill House, Snowdon Drive, Milton Keynes, MK6 1AX, UK (GFN) Corresponding author: e.udovikova@bristol.ac.uk