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  • Title: Gene expression of 3beta-hydroxysteroid dehydrogenase and 17beta-hydroxysteroid dehydrogenase in relation to androstenone, testosterone, and estrone sulphate in gonadally intact male and castrated pigs.
    Author: Chen G, Bourneuf E, Marklund S, Zamaratskaia G, Madej A, Lundström K.
    Journal: J Anim Sci; 2007 Oct; 85(10):2457-63. PubMed ID: 17609472.
    Abstract:
    Androstenone is one of the main compounds responsible for boar taint, and 3beta-hydroxysteroid dehydrogenase (3betaHSD) might be involved in its metabolism. In this study, the gene expression of 3betaHSD and 17beta-hydroxysteroid dehydrogenase (17betaHSD) were determined by real-time PCR analysis and related to the concentrations of androstenone, testosterone, and estrone sulphate (E1S). The experiments were performed on gonadally intact male pigs classified based on high or low fat androstenone concentrations, as predetermined by HPLC, as well as on immunocastrated and surgically castrated male pigs. The male pigs with high androstenone concentrations in fat had low 3betaHSD gene expression in liver and testis. Moreover, the 17betaHSD gene expression in liver, but not in testis, varied negatively with fat androstenone concentrations. Immunocastrated and surgically castrated male pigs had nondetectable concentrations of fat androstenone and plasma testosterone and E1S, and the castration procedure induced a significant increase of 3betaHSD and 17betaHSD gene expression. The mRNA expression was generally much greater from the 3betaHSD than from the 17betaHSD gene. Furthermore, fat androstenone was negatively correlated with liver 3betaHSD gene expression (Pearson correlation, r = -0.69; P < 0.05), and the 17betaHSD gene expression in liver was negatively correlated with plasma E1S (r = -0.95; P < 0.001), indicating an important role of liver 17betaHSD in the estrogen metabolism of gonadally intact male pigs. Another strong correlation was found between 3betaHSD and 17betaHSD gene expression in liver of the gonadally intact male pigs (r = 0.86; P < 0.01), possibly reflecting similar regulation mechanisms of these genes.
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