Efficacy of guanidinoacetic acid supplementation in diets with various energy contents on growth performance, intestinal morphology, serum biochemical parameters and antioxidant status of broilers under dexamethasone-induced oxidative stress

Glucocorticoid-induced oxidative stress impairs growth performance and metabolic homeostasis in broiler chickens, and these adverse effects may be exacerbated by reduced dietary energy. This study investigated whether dietary guanidinoacetic acid (GAA) supplementation could alleviate dexamethasone (DEX)-induced physiological disturbances under different dietary apparent metabolisable energy (AME) levels. A total of 1008 Ross 308 male broilers were assigned to a 2 × 3 × 2 factorial arrangement consisting of two dietary AME levels (standard or low), three GAA concentrations (0, 0.6, and 1.2 g/kg), and two DEX challenge conditions (0 or 1 mg/kg). Significant AME × GAA × DEX interactions were detected for growth performance, jejunal morphology, serum biochemical indices, antioxidant status, and heterophil-to-lymphocyte ratio (H/L). DEX impaired growth performance, with greater reductions under the low-energy diet (p < 0.05). Compared with the unchallenged standard-energy control, daily weight gain decreased by 66.6% and feed conversion ratio (FCR) increased by 132% in DEX-challenged broilers fed the low-energy diet (p < 0.05). Under these conditions, 0.6 g/kg GAA improved FCR by 4.3%, whereas 1.2 g/kg restored villus height and villus-height-to crypt depth ratio to values comparable with DEX-challenged birds fed the standard-energy diet and reduced serum cholesterol, low density lipoprotein, and alanine amino transferase (p < 0.05). GAA also attenuated the DEX-induced increase in H/L but did not improve post-challenge growth recovery. Overall, GAA efficiency depended on dietary energy density, with supplementation being most beneficial during glucocorticoid challenge under low-energy feeding, where 0.6 g/kg primarily improved feed efficiency and 1.2 g/kg elicited greater improvements in intestinal morphology and metabolic responses.