The yellow drum Nibea albiflora is a marine fish of great economic value in China. Despite efforts to improve yields, aquaculture of this species has been hindered by increases in winter-related mortalities associated with cold temperatures and associated natural fasting periods. To better understand the molecular mechanisms that regulate stress responses in yellow drum during periods of cold and starvation, the effect of these stresses on the liver was investigated by performing comparative analyses among fish subjected to different temperatures and feeding strategies. The experiment lasted for 22 d and involved 4 groups: one fed group (control) and one fasted group at 16°C, and one fed group and one fasted group at 8°C. Our results showed that all stress-treated groups exhibited body weight loss during the experiment, demonstrating that both cold stress and fasting caused growth inhibition, but only the fish in the fasted group at 16°C showed a loss in the liver/body ratio, suggesting that starvation can cause mass loss in the liver while cold stress can result in mass loss in both liver and other tissues. Histological alterations were observed in the liver cells from stress-treated groups, also indicating mass loss in the liver during cold stress and starvation. Transcriptomic analysis showed that genes related to the meta bolism of carbohydrates, lipids and amino acids were the most enriched differentially expressed genes during the challenge conditions. These findings can help reveal molecular mechanisms regulating the stress responses of yellow drum exposed to cold and starvation.

中文翻译：

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寒冷和饥饿对黄鼓Nibea albiñora肝脏的影响：组织学改变和转录组学分析

黄鼓鲀是我国具有重要经济价值的海洋鱼类。尽管努力提高产量，但由于与低温和相关的自然禁食期相关的冬季相关死亡率增加，该物种的水产养殖受到阻碍。为了更好地了解在寒冷和饥饿期间调节黄鼓应激反应的分子机制，通过对不同温度和饲养策略的鱼进行比较分析，研究了这些应激对肝脏的影响。实验时间为22 d，共4组：16℃摄食组（对照组）和禁食组1组，8℃摄食组和禁食组1组。我们的结果表明，所有压力治疗组在实验过程中都表现出体重减轻，证明冷应激和禁食都会导致生长抑制，但只有 16°C 禁食组的鱼表现出肝/体比的损失，这表明饥饿会导致肝脏质量损失，而冷应激会导致质量下降。肝脏和其他组织的损失。在来自应激治疗组的肝细胞中观察到组织学改变，这也表明在冷应激和饥饿期间肝脏的质量损失。转录组学分析表明，在挑战条件下，与碳水化合物、脂质和氨基酸代谢相关的基因是最丰富的差异表达基因。这些发现有助于揭示调节暴露于寒冷和饥饿的黄鼓应激反应的分子机制。但只有 16°C 禁食组的鱼表现出肝脏/身体比例的下降，这表明饥饿会导致肝脏质量损失，而冷应激会导致肝脏和其他组织的质量损失。在来自应激治疗组的肝细胞中观察到组织学改变，这也表明在冷应激和饥饿期间肝脏的质量损失。转录组学分析表明，在挑战条件下，与碳水化合物、脂质和氨基酸代谢相关的基因是最丰富的差异表达基因。这些发现有助于揭示调节暴露于寒冷和饥饿的黄鼓应激反应的分子机制。但只有 16°C 禁食组的鱼表现出肝脏/身体比例的下降，这表明饥饿会导致肝脏质量损失，而冷应激会导致肝脏和其他组织的质量损失。在来自应激治疗组的肝细胞中观察到组织学改变，这也表明在冷应激和饥饿期间肝脏的质量损失。转录组学分析表明，在挑战条件下，与碳水化合物、脂质和氨基酸代谢相关的基因是最丰富的差异表达基因。这些发现有助于揭示调节暴露于寒冷和饥饿的黄鼓应激反应的分子机制。表明饥饿会导致肝脏的质量损失，而冷应激会导致肝脏和其他组织的质量损失。在来自应激治疗组的肝细胞中观察到组织学改变，这也表明在冷应激和饥饿期间肝脏的质量损失。转录组学分析表明，在挑战条件下，与碳水化合物、脂质和氨基酸代谢相关的基因是最丰富的差异表达基因。这些发现有助于揭示调节暴露于寒冷和饥饿的黄鼓应激反应的分子机制。表明饥饿会导致肝脏的质量损失，而冷应激会导致肝脏和其他组织的质量损失。在来自应激治疗组的肝细胞中观察到组织学改变，这也表明在冷应激和饥饿期间肝脏的质量损失。转录组学分析表明，在挑战条件下，与碳水化合物、脂质和氨基酸代谢相关的基因是最丰富的差异表达基因。这些发现有助于揭示调节暴露于寒冷和饥饿的黄鼓应激反应的分子机制。转录组学分析表明，在挑战条件下，与碳水化合物、脂质和氨基酸代谢相关的基因是最丰富的差异表达基因。这些发现有助于揭示调节暴露于寒冷和饥饿的黄鼓应激反应的分子机制。转录组学分析表明，在挑战条件下，与碳水化合物、脂质和氨基酸代谢相关的基因是最丰富的差异表达基因。这些发现有助于揭示调节暴露于寒冷和饥饿的黄鼓应激反应的分子机制。