To explore the effect of density on large yellow croaker (Larimichthys crocea) under intensive aquaculture conditions and determine the appropriate culturing density, this study investigate the effects of different stocking densities on the nutritional composition, stress, and immune levels of large yellow croaker. Through a long-term aquaculture experiment, conducted under flow-through conditions of intensive aquaculture, three initial density groups were set: a low density group [LD], 4.92 kg/m³; a medium density group [MD], 7.56 kg/m³; and a high density group [HD], 10.08 kg/m³, for a 150-day rearing trial. Large yellow croaker were fed to satiation twice daily (6:00, 17:00). At the end of this trial, the final densities were 10.38 ± 0.50, 14.41 ± 1.06, and 18.71 ± 0.99 kg/m³ in the LD, MD, and HD groups, respectively. The results showed that the growth performances were adversely influenced by a high stocking density. Levels of cortisol in serum, superoxide dismutase (SOD) and catalase (CAT) in liver, Na⁺-K⁺ ATPase and Na⁺-K⁺ ATPase gene in gills, and heat shock protein (HSP70/90) genes and glutathione S-transferase (GST) genes in the liver significantly increased under HD treatment. Results of immune response analyses showed that there was a clear decrease in immunoglobulin M (IgM), complement component 4 (C4), and lysozyme (LZM) in serum, lysozyme (LZM) genes, tumor necrosis factor-alpha (TNF-α) genes and interleukin-1β (IL-1β) genes in the head kidney of large yellow croakers reared in the HD group. An obvious increase in free amino acids and fatty acids in the muscle of large yellow croakers reared in HD group was also observed. Overall, this study showed that the optimal final culturing density of large yellow croaker under flow-through systems should be between 14.41 kg/m³ and 18.71 kg/m³ to improve aquaculture efficiency and product quality.

To optimize all‐female production in marbled flounder ( Pseudopleuronectes yokohamae ), a species with marked female‐biased growth, hormonal induction of pseudomales using 17 α ‐methyltestosterone (MT) is essential. However, its impact on somatic growth is dose‐dependent, and the underlying mechanisms remain poorly understood. This study employed transcriptome sequencing of muscle and liver to decipher the molecular basis of growth regulation in juveniles fed diets containing 0, 0.5, or 2.0 mg/kg MT. Phenotypically, the 0.5 mg/kg dose sustained growth, while the 2.0 mg/kg dose caused significant inhibition, aligning with prior data. RNA‐seq revealed a hierarchical transcriptional response. The low dose induced modest changes primarily in metabolic and signaling pathways. Strikingly, the high dose triggered a potent, coordinated activation of core anabolic and proliferative pathways (e.g., cell cycle, ribosome biogenesis, and aminoacyl‐tRNA biosynthesis) in both tissues. Crucially, this activation in muscle was paralleled by a pronounced suppression of the systemic growth hormone/insulin‐like growth factor (GH/IGF) axis, evidenced by the downregulation of igf1 and ghr . This conflict between activated cellular biosynthesis and repressed endocrine growth signaling provides a direct mechanistic explanation for the high‐dose growth inhibition. Tissue specialization was evident: muscle transcriptomes emphasized structural construction, whereas hepatic responses centered on metabolic reprogramming and proliferation. Key gene expression trends were validated by qRT‐PCR. Our findings elucidate that the growth‐suppressive effect of high‐dose MT originates from a maladaptive transcriptional imbalance. They provide a strong molecular rationale for employing the 0.5 mg/kg MT dosage to achieve effective sex reversal without compromising growth in marbled flounder aquaculture.

Triploid turbot (Scophthalmus maximus) exhibit superior growth and survival, yet the molecular basis of their sterility—a key trait for aquaculture—remains largely unexplored. This study investigated ovarian development and transcriptomic profiles in diploid and triploid S. maximus at three key stages (6, 10, and 20 months post-hatch, mph) to elucidate the stage-specific molecular mechanisms underlying triploid sterility. Histological analysis revealed that diploid ovaries progressed through normal oogenesis to the early vitellogenic stage by 20 mph, whereas triploid ovaries were arrested at the oogonial stage, with only occasional primary oocytes and extensive connective tissue infiltration. Comparative transcriptomic analysis identified 13,305, 14,599, and 13,331 differentially expressed genes (DEGs) between triploid and diploid ovaries at 6, 10, and 20 mph, respectively. Functional enrichment analysis showed that DEGs were significantly associated with meiotic processes, cell cycle regulation, energy metabolism, and apoptosis. Key meiotic genes (spo11, dmc1, sycp3) were consistently upregulated in triploids across all stages, while the DNA repair gene rad51 was paradoxically downregulated, indicating attempted but aberrant meiotic initiation. Oogenesis regulators (gdf9, bmp15, pou5f3) and energy metabolism genes (ndufa11, sdha, cox5a) were significantly downregulated, whereas apoptosis-related genes (eif2ak3, apaf1) were upregulated. Notably, KEGG pathway analysis revealed stage-specific shifts from stress-induced apoptosis and p53 signaling at early stages to proteasome activation at later stages, suggesting a transition from active germ cell elimination to maintenance of cellular homeostasis in developmentally arrested ovaries. Collectively, these findings demonstrate that triploid sterility is associated with coordinated dysregulation of meiotic progression, metabolic, and apoptotic pathways, providing a high-resolution molecular framework for understanding reproductive failure in triploid fish and informing strategies for optimizing triploid production in aquaculture.