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.).

Abstract

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℃, 29℃, and 33℃ 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℃ 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℃ and 29℃ groups. However, there were no significant differences between the 25℃ and 29℃ groups. The most severe damage to liver tissue was observed in the 33℃ 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℃ 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℃ group. In contrast, the expression of the glycolysis pathway-related gene (pyruvate kinase (Pk)) was up-regulated. In addition, the expressions of fatty acid β oxidation pathway-related genes (peroxisome proliferator-activated receptor-Alpha (Pparα) and carnitine palmityl transferase 1 (Cpt1)), adipogenesis pathway-related genes (peroxisome proliferator-activated receptor-Gamma (Pparγ), 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.