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Chronic heat stress is capable of reducing the growth performance, causing damage to the liver structure, and altering the liver glucose metabolism and lipid metabolism in largemouth bass (Micropterus salmoides L.)

文献类型: 外文期刊

作者: Yan, Hanwei 1 ; Du, Jinxing 1 ; Li, Shengjie 1 ; Lei, Caixia 1 ; Zhu, Tao 1 ; Han, Linqiang 3 ; Song, Hongmei 1 ;

作者机构: 1.Chinese Acad Fisheries Sci, Pearl River Fisheries Res Inst, Key Aboratory Trop & Subtrop Fishery Resource Appl, China Minist Agr, Guangzhou 510380, Peoples R China

2.Shanghai Ocean Univ, Coll Fisheries & Life Sci, Shanghai 201306, Peoples R China

3.Guangdong Liangshi Aquat Seed Ind Co Ltd, Foshan 528100, Peoples R China

关键词: Largemouth bass; Chronic heat stress; Growth performance; Liver damage; Glucose metabolism; Lipid metabolism

期刊名称:FISH PHYSIOLOGY AND BIOCHEMISTRY ( 影响因子:2.5; 五年影响因子:3.1 )

ISSN: 0920-1742

年卷期: 2025 年 51 卷 1 期

页码:

收录情况: SCI

摘要: High temperatures cause abnormal energy metabolism and inhibit the growth of fish in aquaculture. However, the mechanism of energy metabolism under chronic heat stress is still unknown. In this study, largemouth bass (Micropterus salmoides, LMB) was treated with 25 degrees C, 29 degrees C, and 33 degrees C for 8 weeks. Then, the growth performance, liver tissue damage, serum lipid indicator, hepatic glycogen, and triglyceride levels were analyzed. The growth data showed that the 33 degrees C group had a lower weight gain rate (WGR), specific growth rate (SGR), feeding rate (FR), and higher feed conversion rate (FCR) in comparison with those in the 25 degrees C and 29 degrees C groups. However, there were no significant differences between the 25 degrees C and 29 degrees C groups. The most severe damage to liver tissue was observed in the 33 degrees C group, characterized by cellular vacuolation and marginalization of cell nuclei. The levels of triglyceride, total cholesterol, high-density lipoprotein cholesterol, and low-density lipoprotein cholesterol in the serum were decreased with the rising temperatures. However, the hepatic triglyceride levels were increased, with a decrease in hepatic glycogen levels. Compared with the 25 degrees C group, the expressions of gluconeogenesis pathway-related genes (phosphoenolpyruvate carboxykinase (Pepck) and glucose-6-phosphatase (G6pase)) and glucose transport pathway-related gene (glucose transporter 2 (Gltu2)) were down-regulated in the 33 degrees C group. In contrast, the expression of the glycolysis pathway-related gene (pyruvate kinase (Pk)) was up-regulated. In addition, the expressions of fatty acid beta oxidation pathway-related genes (peroxisome proliferator-activated receptor-Alpha (Ppar alpha) and carnitine palmityl transferase 1 (Cpt1)), adipogenesis pathway-related genes (peroxisome proliferator-activated receptor-Gamma (Ppar gamma), fatty acid synthase (Fas), acetyl-CoA carboxylase (Acc)), and lipolysis pathway-related genes (adipose triglyceride lipase (Agtl) and hormone-sensitive lipase (Hsl)) were down-regulated under chronic heat stress. In conclusion, our results indicated that enhancement of the glycolysis pathway and inhibition of the gluconeogenesis pathway and lipid metabolism contribute to coping with chronic heat stress for LMB. Our study provides useful information for alleviating the heat stress response of LMB through nutritional regulation in the future.

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