AMPK-mediated energetic metabolism regulates compensatory growth in fasting-refeeding juvenile mandarin fish (Siniperca chuatsi)

Juvenile mandarin fish experience fasting stress during artificial diet domestication, yet its physiological responses and compensatory growth mechanism remain unclear. This study subjected 1.5-month-old fish to fasting (3d, 7d, 16d, 25d) followed by refeeding (1d, 7d, 20d). Growth performance, energy reserves, and expression levels of AMP-activated protein kinase (AMPK) (ampk α1/α2) in liver and muscle were analyzed. Results revealed that prolonged fasting progressively reduced body weight, hepatosomatic index, hepatic glycogen, and triglycerides, while muscle glycogen remained stable. Muscle amino acids were initially maintained but mobilized after extended fasting. Hepatic and muscular ampk α1/α2 expression was up-regulated during the initial stages of fasting but down-regulated as fasting prolonged. This indicates that early fasting activated AMPK to mobilize hepatic energy stores. However, prolonged fasting suppressed AMPK, suggesting the body entered a low-energy state, during which muscle amino acids were utilized. Early refeeding downregulated ampk α1/α2, coincided with the replenishment of glycogen and lipid. By refeeding 20d, all fasted groups restored energy reserves. The fasted 3d and 7d groups achieved complete compensatory growth with normalized AMPK signaling in muscle. In contrast, the fasted 16d and 25d groups showed only partial compensatory growth, with persistently elevated AMPK levels, indicating unresolved energy stress. These findings demonstrate that fasting activates the AMPK pathway to prioritize hepatic glycogen/lipid catabolism, while refeeding shifts metabolic equilibrium toward anabolism via AMPK suppression. However, prolonged fasting (16–25d) induced persistent energy deficits, impairing full weight recovery. Practically, mandarin fish refusing artificial diets should be promptly resume live bait to minimize losses.