Mechanistic insight into the role of immunocastration on eliminating skatole in boars.

The accumulation of skatole in fat tissue is one of the predominant factors, causing boar taint. The present study was aimed to understand the mechanism whereby active immunization against GnRH (immunocastration) eliminates skatole in boars. Thirty-six boars were assigned within litter into three groups (n = 12): control, surgically castrated, or immunized against GnRH at 10 wk of age (with a booster 8 wk later). Faecal and blood samples (for skatole and skatole-regulatory hormone profiles) were collected at 4-wk intervals until boars were slaughtered (26 weeks). Immunocastration reduced (P < 0.05) serum levels of androstenone, 17β-estradiol and IGF1 especially after the booster immunization, and down-regulated (P < 0.05) mRNA expressions of both IGF1 and IGF1receptor (IGF1R) in mucosa of ileum as well as colon at slaughter. Compared to intact controls, immunocastration substantially decreased (P < 0.05) faecal skatole contents subsequent to the decrease of serum IGF1 levels, which persisted in boars after surgical castration. In parallel with the decreased formation of skatole in the intestine, levels of skatole in serum and then in fat tissue were also decreased (P < 0.05). On the other hand, deprivation of testicular steroids, especially androstenone and 17β-estradiol accelerated skatole degradation metabolism in the liver by increasing (P < 0.05) hepatic CYP2E1, CYP2A, CYP2C49 and CYB5A expressions. Collectively, our results suggested that immunocastration decreased skatole formation in the intestine and meanwhile accelerated skatole degradation metabolism in the liver, resultantly eliminating skatole accumulation in male pigs. Decreased intestinal skatole formation by immunocastration appeared to be associated with the attenuated actions of IGF1 on the turnover of both ileal and colon mucosa.