Plasma metabolomic profiling reveals metabolic shifts linked to growth depression in broilers fed high level of valine.

A study was conducted to investigate the changes of plasma metabolome profiles by which excessive dietary valine modulates the body weight in broilers. A total of 960 male day-old Ross 708 broilers were randomly assigned to two dietary treatments (100% vs. 150% of valine supplementation diet) with 24 replicates per treatment. Corn-soybean meal-based diets were provided until d 42, and plasma samples were collected on d 14 and 42 for untargeted metabolomic profiling. On d 14, 150% valine significantly increased plasma valine concentrations compared with the 100% valine group (False Discovery Rate; FDR < 0.05), with no observed changes in other metabolites or body weight. On d 42, the 150% valine group showed significantly increased plasma valine concentrations (FDR < 0.001) and reduced body weight (P = 0.018) compared with the 100% valine group. Plasma concentrations of leucine and isoleucine were significantly decreased in the 150% group (FDR < 0.05). A significant positive correlation was observed between plasma leucine concentration and body weight (r = 0.29, P = 0.045). Furthermore, plasma concentrations of methylmalonic acid (MMA), 2-hydroxyisovaleric acid (2-HIVA), and alpha-ketoglutarate were significantly increased in the 150% valine group compared to the 100% valine group (FDR < 0.05). MMA (r = -0.34, P = 0.019) and 2-HIVA (r = -0.30, P = 0.040) showed significant negative correlations with body weight. Plasma concentrations of gamma-tocopherol and aspartate were significantly reduced in the 150% valine group on d 42 (FDR < 0.05). Plasma gamma-tocopherol showed a significant positive correlation with body weight (r = 0.34, P = 0.018) and a significant negative correlation with plasma valine (r = -0.43, P = 0.010). In conclusion, the current study indicates that 150% valine acts as a potent metabolic stressor in broiler chickens. This growth depression is driven by branched-chain amino acid antagonism, followed by catabolic byproduct accumulation and subsequent exhaustion of the antioxidant defense system.