46. Effects of Fermentable Carbohydrates on Boar Taint and Fecal Short-chain Fatty Acid Profiles in Intact Male Pigs.

Abstract The objective of this study is to determine whether dietary supplementation with fermentable carbohydrate sources, raw potato starch (RPS) or sugar beet pulp (SBP), alters androstenone concentrations, individual response phenotypes, and fecal short-chain fatty acid (SCFA) profiles in intact male pigs. Boar taint, primarily caused by the accumulation of androstenone and skatole in adipose tissue, limits the production of intact males despite advantages in growth performance, feed efficiency, and lean yield. Fermentable carbohydrates modify hindgut fermentation and increase SCFA production, which may influence the metabolism and clearance of boar taint compounds. Therefore, two fermentable carbohydrate sources with different fermentation characteristics, RPS and SBP, were selected to evaluate diet-induced differences in endocrine and fermentation responses. Thirty-two intact male pigs (initial body weight = 70.41 ± 0.86 kg) were fed a control diet during a one-week acclimation period, followed by a four-week treatment phase in which pigs received diets containing either 5% RPS or 5% SBP. Pigs were then returned to the control diet for a two-week recovery phase to determine whether boar taint developed after treatment removal. Blood and fecal samples were collected weekly, and backfat samples were collected biweekly throughout the trial. Concentrations of SCFA and androstenone were quantified using high-performance liquid chromatography and enzyme-linked immunosorbent assay. Statistical analyses were conducted in R using a linear mixed-effects model to evaluate the effects of diet, timepoint, and their interaction on SCFA and androstenone concentrations. Androstenone concentrations changed significantly over time during the trial (P < 0.01). Based on androstenone concentrations relative to the boar taint threshold, pigs were classified into three phenotypes: responders that responded to treatment, non-responders that did not respond to treatment, and no-taint animals that never developed boar taint. Of the 32 boars, 59.4% did not develop boar taint, 28.1% responded to the treatment, and 12.5% did not respond. Responders maintained androstenone concentrations below the boar taint threshold during the dietary treatment phase but exceeded the threshold after pigs returned to the control diet during the recovery phase (P < 0.001). In contrast, non-responders exhibited greater androstenone concentrations during the treatment phase, whereas no-taint pigs maintained consistently low concentrations throughout the study. Among responders, 66.7% were fed RPS, whereas 33.3% were fed SBP, indicating that a greater proportion of responders was observed in pigs fed RPS. Fecal SCFA concentrations varied across sampling weeks (P < 0.05), with acetate, propionate, and butyrate concentrations reaching their peak at mid-treatment (P < 0.05). Similar temporal patterns were observed at mid-recovery, indicating shifts in gut fermentation during dietary supplementation (P < 0.05). These results highlight substantial individual variability in boar taint development and suggest that boar taint mitigation strategies may need to account for distinct response phenotypes.