Chronic Cortisol Exposure Drives Tissue-Specific Redox Imbalance, Metabolic Remodeling, Growth Inhibition, and Impaired Feeding Recovery in Golden Pompano (Trachinotus blochii)

Chronic stress is a pervasive challenge in intensive aquaculture, particularly for fast-growing and metabolically active species such as golden pompano (Trachinotus blochii), which is highly sensitive to environmental stress. However, the mechanisms linking sustained cortisol elevation to impaired growth remain poorly understood. Juvenile golden pompano were fed a control diet, a diet supplemented with hydrocortisone sodium succinate, or a diet containing the glucocorticoid receptor (GR) antagonist AL082D06 for 90 days. Growth, redox status, metabolism, tissue responses, and feeding behavior were assessed. Chronic cortisol treatment significantly reduced growth, condition factor, and mesenteric fat index and increased plasma glucose, non-esterified fatty acids, and β-hydroxybutyrate. In liver and muscle, cortisol increased ROS, MDA, SOD, and GSH levels and decreased CAT and GSH-Px activities. These changes, together with elevated plasma AST and ALT activities, indicated redox imbalance and tissue injury. Lipid deposition decreased, whereas glycogen accumulated in both tissues. Multi-omics analyses revealed broader metabolic responses in liver than in muscle, involving lipid, carbohydrate, and amino acid metabolism and stress-related signaling. Cortisol-treated fish also showed prolonged feeding time, delayed post-stress feeding, and increased avoidance behavior. AL082D06 increased tissue lipid and glycogen stores but also increased lipid peroxidation. These findings link chronic cortisol exposure to tissue-specific redox imbalance and metabolic remodeling, accompanied by impaired growth and feeding recovery in golden pompano.