Effects of artificial diet on glycolytic pathway and immune response in mandarin fish (Siniperca chuatsi)

Mandarin fish (Siniperca chuatsi) is a carnivorous species of significant interest in aquaculture. Although advances have been made in developing formulated diets, transitioning from live prey (LP) to artificial feed (FP) often induces metabolic dysfunction. This study comprehensively compared physiological responses between LP and FP-fed groups, analyzing hematological parameters, serum biochemistry, hepatic metabolism, and immune-related gene expression. Results indicated that FP feeding induced marked physiological alterations: significant reduction in red blood cells (RBC), white blood cells (WBC), and hemoglobin (Hb), alongside elevated mean corpuscular hemoglobin concentration (MCHC). Immunological profiling revealed a dysregulated inflammatory response, characterized by upregulated pro-inflammatory IL-6, and down-regulated IL-1β, IL-8, and TNF-α expression, coupled with decreased anti-inflammatory IL-10, and toll-like receptors (TLR1, TLR2). Concurrently, serum IgM and CD4 activity significantly increased. FP-fed fish exhibited hyperglycemia (p < 0.01), and significantly diminished T-AOC and SOD activity, indicating systemic oxidative stress. Further, hepatic analysis confirmed metabolic disruption, with considerably elevated glucose and glycogen content. Despite increased levels of glycolytic intermediates (Glucose-6-phosphate, Pyruvate), the activities of key rate-limiting enzymes (HK, PFK-1, and PK) were significantly suppressed. Hepatic tissue displayed pathological enlargement, vacuolization, and structural irregularity. We conclude that formulated diet feeding disrupts metabolic homeostasis, primarily by inhibiting hepatic glycolysis, leading to glucose accumulation, oxidative stress, and subsequent immune imbalance. This study provides fundamental data for developing nutritional strategies to mitigate metabolic syndrome in farmed mandarin fish.