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In the present study, we evaluated the effects of various stocking densities on the tracheal barrier and plasma metabolic profiles of finishing broilers. We randomly assigned 1,440 Lingnan Yellow feathered broilers (age 22 d) to 5 different stocking density groups (8 m−2, 10 m−2, 12 m−2, 14 m−2, and 16 m−2). Each of these consisted of 3 replicates. The interleukin (IL)-1β and IL-10 concentrations were substantially higher in the 16 m−2treatment group than they were in the 8 m−2and 10 m−2treatment groups (P < 0.05). Nevertheless, IL-4 did not significantly differ among the 5 treatments (P > 0.05). The tracheal mucosae of the birds in the 16 m−2group (high stocking density, HSD) were considerably thicker than those for the birds in the 10 m−2group (control, CSD). Relative to CSD, the claudin1 expression level was lower, and the muc2 and caspase3 expression levels were higher for HSD. Compared with CSD, 10 metabolites were significantly upregulated (P < 0.05), and 7 were significantly downregulated (P < 0.05) in HSD. Most of these putative diagnostic biomarkers were implicated in matter biosynthesis and energy metabolism. A metabolic pathway analysis revealed that the most relevant and critical biomarkers were pentose and glucuronate interconversions and the pentose phosphate pathway. Activation of the aforementioned pathways may partially counteract the adverse effects of the stress induced by high stocking density. This work helped improve our understanding of the harmful effects of high stocking density on the tracheal barrier and identified 2 metabolic pathways that might be associated with high stocking density–induced metabolic disorders in broilers.

There is no information regarding the influence of heat stress (HS) on host metabolic profile. In this study, we investigated the effects of different environmental temperatures on oxidative status, hormone levels, HS indicators, and plasma metabolites in broilers. A total of 1,680 yellow-feather broilers (28 D old) were randomly allotted to 4 groups with 6 replicates. The broilers (29–57 D old) were maintained in thermostatic rooms (20°C, 25°C, 28°C, and 30°C) for 28 consecutive days. The results showed that the plasma cortisol and adrenocorticotropic hormone levels and creatine kinase and lactate dehydrogenase activities gradually increased when the temperature increased from 20°C to 30°C. However, the insulin-like growth factor-І level decreased gradually. Furthermore, heat shock protein 70 expression significantly increased in the liver and breast muscle (P < 0.01). As the temperature increased, the total anti-oxidant capacity in the plasma and liver gradually decreased, whereas the malondialdehyde level increased. The activity of plasma glutathione peroxidase and total superoxide dismutase in the liver showed a similar increasing trend (P < 0.01). In addition, 15 metabolites were identified at higher (P < 0.05) levels, whereas 2 metabolites were identified at lower (P < 0.05) levels in the 30°C treatment group than those in the 25°C treatment group. Most of these potentially diagnostic biomarkers are involved in carbohydrate, amino acid, lipid, or gut microbiome-derived metabolism, indicating that HS affected the metabolic pathways in broilers. Six candidate metabolites (tartronic acid, l-bethreine, tartaric acid, allose, glutaric acid, and neohesperidin) were selected as biomarkers, as they showed high sensitivity, specificity, and accuracy in diagnosing broilers under HS (P < 0.01). In conclusion, in the final stage of growth, we identified 6 plasma differential metabolites as potential biomarkers of HS-induced metabolic disorders in yellow-feathered broilers. This work offers new insights into the metabolic alterations of broilers exposed to HS and provides a new perspective for further study.