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.
Boar taint is a meat quality issue characterized by an off-odour or off-flavour in pork caused by the accumulation of androstenone in the fat. Our previous work demonstrated that androstenone binds non-specifically to albumin in the plasma and suggested that the binding affinity of androstenone might vary between individual animals, which may affect the subsequent development of boar taint. Therefore, the purpose of this study was to characterize the binding of androstenone in the plasma of animals with high and low fat androstenone concentrations to determine the effect of androstenone binding affinity on the development of boar taint. Plasma and backfat samples were obtained from 5-month-old terminal cross [Duroc x (Landrace x Yorkshire)] (n = 8) boars. An androstenone specific enzyme-linked immunosorbent assay (ELISA) was used to determine animals with high (n = 4) or low (n = 4) fat androstenone concentrations. The plasma from each boar was incubated with radiolabeled [3H]-androstenone in the presence or absence of excess unlabeled androstenone. Excess unlabeled androstenone created competition for binding sites allowing the displacement of [3H]-androstenone from albumin to be quantified. Incubations were analyzed by a novel high-performance liquid chromatography (HPLC) method we previously developed to assess androstenone binding. Statistical analysis was conducted using a two-way ANOVA. The plasma albumin concentrations were similar across individual boars; however, the percentage of androstenone that could be displaced from albumin in boars with high fat androstenone concentrations ranged from 7.1 ± 2.4% to 21.9 ± 5.2%, and was significantly lower (P = 0.01) than the percentage of androstenone displaced in the animals with low fat androstenone concentrations. These results suggest that the binding affinity of androstenone is inversely related with fat androstenone concentrations, demonstrating for the first time that the transport of androstenone in the plasma may contribute to the development of boar taint.
Boar taint is a meat quality issue characterized by an off-odour or off-flavour in pork caused primarily by the accumulation of androstenone in the fat, but sensory estimates of boar taint do not always correlate with fat androstenone concentrations. However, these evaluations examine the sensory qualities of both the fat and lean tissue of heated pork products. Sulfated metabolites of androstenone are polar compounds that are abundantly produced by the Leydig cells of the testes, which may accumulate in more hydrophilic lean tissue. Therefore, the purpose of this study was to investigate the testicular metabolism of androstenone, which is responsible for the high production of sulfated androstenone metabolites. Leydig cells were isolated from 7-month-old Yorkshire, Duroc and terminal cross [Duroc x (Landrace x Yorkshire)] (n = 3) boars and incubated with radiolabeled androstenone for 8 hours. The proportion of sulfated metabolites produced was quantified using reverse phase high performance liquid chromatography (HPLC) and radioisotope detection. The sulfated metabolites were subsequently identified using liquid chromatography-mass spectrometry (LC-MS/MS). Statistical analysis was conducted using a one-way ANOVA in SAS. Following isolation and analysis with LC-MS/MS, the sulfated metabolites were identified as androstenol-3-sulfate and two major sulfated forms of androstenone. Additionally, removal of the sulfate group from these two sulfated forms of androstenone returned the parent compound androstenone, and not a hydroxylated metabolite. The average production of sulfated androstenol produced across all boars was 52.1±8.6%, which was not significantly different (P = 0.7) from the average production of sulfated androstenone (47.9±8.6%). The results of this study indicate that androstenone is directly sulfated, which allows these sulfated metabolites to function as steroid reservoirs that can enzymatically regenerate free androstenone within hydrophilic lean tissue. Alternatively, these metabolites may accumulate in the lean tissue, which we are proposing as a novel mechanism that contributes to the development of boar taint.
Castration is a highly invasive procedure performed on male pigs within the first few days after birth. Castration reduces aggressive and sexual behaviours and, more importantly, eliminates the incidence of a meat quality issue called boar taint. Androstenone, one of the boar taint causing compounds, is a steroid hormone produced during puberty in boars, and also during a spike of testicular steroidogenesis at 21 days of age. This peak is thought to mature the hypothalamic-pituitary-gonadal axis; however, 21-day steroid concentrations have not previously been linked to the extent of boar taint development at slaughter. The objective of this research is to determine if androstenone concentrations at 21 days of age can predict boar taint development at slaughter. Crossbred [(YorkshireXLandrace)XDuroc] boars (n = 36) were raised in pens of two females and two males to average market slaughter weight. Blood was taken at 21 days and slaughter, backfat was collected at slaughter. Plasma and fat androstenone concentrations were measured by androstenone-specific ELISA. Data was analyzed using Pearson correlation and ANOVA. Boars >120kg at slaughter showed positive correlation (R=0.54, P =.007) between 21-day plasma androstenone and fat androstenone concentrations at slaughter, and tended to correlate (R=0.40, P =.056) between 21-day plasma androstenone and plasma androstenone concentrations at slaughter. Boars yet to reach 120kg by slaughter did not show correlation (R=0.2, P = .2) between 21-day plasma androstenone and slaughter androstenone concentrations. There was no correlation between age and weight at slaughter, and plasma and fat androstenone concentrations were not different (P >.05) between groups above and below 120kg at slaughter. These results suggest that 21-day plasma androstenone concentrations may be indicative of androstenone accumulation in the fat and plasma if pigs are over 120kg at slaughter. This can aid with identifying boars at risk of developing boar taint early so that solutions such as immunocastration can be implemented.
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