Boar taint is caused by the accumulation of androstenone and skatole and other indoles in the fat; this is regulated by the balance between synthesis and degradation of these compounds and can be affected by a number of factors, including environment and management practices, sexual maturity, nutrition, and genetics. Boar taint can be controlled by immunocastration, but this practice has not been accepted in some countries. Genetics offers a long-term solution to the boar taint problem via selective breeding or genome editing. A number of short-term strategies to control boar taint have been proposed, but these can have inconsistent effects and there is too much variability between breeds and individuals to implement a blanket solution for boar taint. Therefore, we propose a precision livestock management approach to developing solutions for controlling taint. This involves determining the differences in metabolic processes and the genetic variations that cause boar taint in specific groups of pigs and using this information to design custom treatments based on the cause of boar taint. Genetic, proteomic or metabolomic profiling can then be used to identify and implement effective solutions for boar taint for specific populations of animals.
Androstenone circulates in the plasma bound to albumin before accumulating in the fat, resulting in the development of boar taint. Androstenone sulfate is more abundant in the circulation than free androstenone; however, it is unclear how androstenone sulfate is transported in the plasma and if steroid transport affects the development of boar taint. Therefore, the purpose of this study was to characterize the binding of androstenone sulfate in boar plasma and determine if variability in steroid binding affects the accumulation of androstenone in the fat. [3H]-androstenone sulfate was incubated with plasma and the steroid binding was quantified using gel filtration chromatography. Inter-animal variability was assessed by quantifying androstenone binding specificity in plasma obtained from boars that had high or low fat androstenone concentrations at slaughter. Androstenone sulfate bound minimally in the plasma and to isolated albumin, which suggests that it is transported primarily in solution. The specific binding of androstenone quantified in plasma and isolated albumin from low fat androstenone animals was significantly higher (p = 0.01) than in high fat androstenone boars. These results indicate that the binding of androstenone to albumin varies amongst individual animals and affects the transport of androstenone in the plasma and accumulation in the fat of the boar.
Boars express high testicular levels of sulfotransferase enzymes, and consequently, the boar taint causing compound androstenone predominantly circulates as a steroid sulfate. Androstenone sulfate is suspected to function as a steroid reservoir that can be deconjugated to provide a source of free androstenone for accumulation. Therefore, the purpose of this study was to characterize the uptake and deconjugation of androstenone sulfate in the adipose tissue of the boar. Real-time PCR was used to quantify the expression of steroid sulfatase (STS) and several organic anion transporting polypeptides (OATPs) in the adipose tissue. Additionally, [3H]-androstenone sulfate was incubated with adipocytes or supernatant from homogenized fat to assess steroid uptake and conversion, respectively. A positive correlation existed between OATP-B expression and androstenone sulfate uptake (r = 0.86, p = 0.03), as well as between STS expression and androstenone sulfate conversion (r = 0.76, p < 0.001). Moreover, fat androstenone concentrations were positively correlated (r = 0.85, p < 0.001) with androstenone sulfate conversion and tended to increase with STS expression in early maturing boars. This suggests that androstenone sulfate uptake and deconjugation are mediated by OATP-B and STS, respectively, which may influence the development of boar taint in early maturing animals.
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