Effects of benzoic acid or benzocal-50 supplementation on growth performance and intestinal health in mixed-sex Ross 308 chickens under a high stocking density

An experiment was conducted to evaluate the impacts of dietary supplementation with unprotected benzoic acid (BA) or benzocal-50 (protected BA) on the growth performance and intestinal health in mixed-sex Ross 308 broilers under a high stocking density. A total of 768 one-d-old mixed-sex Ross 308 chickens (BW: 43.52 ± 0.68 g) were randomly allotted to 4 treatments (6 replicates with 32 broilers in each): 1) basal diet (NC); 2) basal diet with 30 mg/kg of avilamycin (PC); 3) basal diet with 1,000 mg/kg of BA (PBA); and 4) basal diet with benzocal-50 (330, 330, and 300 mg/kg in the starter (d 1-14), grower (d 15–28), and finisher (d 29–41) phases) (EBA). The normal stocking density during the finisher phase for broilers is 25.0 kg BW/m², but this study used a density of 29.0 kg BW/m² for a high stocking density. The results revealed an increase in the ADG of the EBA treatment compared to the PBA treatment during d 8 to 14 (P < 0.05). In the grower (d 15–28) and finisher (d 29–41) phases, chickens fed the EBA treatment exhibited lower intestinal digesta pH values than those in the NC treatment (P < 0.05). Moreover, the EBA treatment displayed greater AID of dry matter and crude protein than the PC treatment (P < 0.05). The EBA treatment resulted in an upregulation of sodium-dependent neutral amino acid transporter and peptide transporter (PEPT1) mRNA expressions in the jejunum on d 14, an increased sodium-glucose transport protein 1 mRNA expression in the jejunum on d 28, and enhanced PEPT1 mRNA expression in the jejunum on d 41, when compared to the NC treatment (P < 0.05). Moreover, the EBA treatment improved cadherin 1 mRNA expression in the jejunum on d 28 than the NC and PC treatments (P < 0.05). Overall, supplementing benzocal-50 to broilers under a high stocking density led to a decrease in gut pH, contributing to reduced fecal score and an overall enhancement in the gut barrier function.