Page 114 - 《水产学报》2026年第3期

3 期 水 产 学 报 50 卷

Chronic heat stress induces hepatic glycolipid abnormal deposition and
mitochondrial dysfunction in Micropterus salmoides

1,2*
1,2
1,2
1,2
WANG Xiaoran , ZENG Weiwei , JIANG Hui , LIU Yu , DENG Junming 3*
(1. School of Animal Science and Technology, Foshan University, Foshan 528231, China;
2. Guangdong Key Laboratory of Animal Molecular Design and Precision Breeding,
Foshan University, Foshan 528225, China;
3. College of Fisheries, Guangdong Ocean University, Zhanjiang 524088, China)

Abstract: With worsening global greenhouse effect, aquaculture faces growing high-temperature threats. Mass mortality events
of farmed fish induced by chronic heat stress (CHS) have become common. Therefore, more attention should be paid to CHS.
To investigate the effects of CHS on carbohydrate and lipid metabolism, as well as mitochondrial homeostasis in fish, a total of
240 juvenile Micropterus salmoides with an average body weight of (12.04±0.15) g were randomly divided into two groups,
each consisting of four replicates. The fish were cultured in thermostatically controlled aquaculture tanks at (27.0±0.5) ℃ (Con-
trol group) and (33.0±0.5) ℃ (Heat group) for 8 weeks, using commercial feed. The results demonstrated that in the Heat
group, the hepatic expression levels of glucose metabolism-related genes, including IRA, IRB, IRS1, PEPCK, GSK3β, AKT1,
and PBP1, were significantly downregulated. Among lipid metabolism-related genes, FAS, LPL, and HSL were significant
downregulated, whereas CPT-1, FFAR, ACC, and ATGL were marked upregulated. Among genes related to mitochondrial
homeostasis, SIRT1 and AMPKα were significantly upregulated, while PGC-1α, ERRα, TFAM7, OAP1, DRP1, P62, LC3, and
MFN1 also showed marked downregulation. In addition, the expression levels of IκBβ, P65, Iκκβ, and IL-8 were all signific-
antly downregulated in the Heat group. Furthermore, the Heat group exhibited abnormal glycogen accumulation and lipid
deposition in the liver, accompanied by mitochondrial structural damage and a significant decrease in mitochondrial density.
Liver transcriptome sequencing revealed that differentially expressed genes were primarily enriched in the C-type lectin
receptor signaling pathway, cytokine-cytokine receptor interaction, actin cytoskeleton regulation, carbon metabolism, and gly-
colysis/gluconeogenesis signaling pathway. In summary, CHS disrupts mitochondrial dynamics homeostasis, induces mito-
chondrial dysfunction and energy metabolic imbalance in M. salmoides. Additionally, CHS disrupts hepatic carbohydrate and
lipid metabolism, leading to abnormal accumulation of glycogen and lipids in the liver. The suppression of energy metabolic
homeostasis by CHS further impairs hepatic immune function in this species. The findings of this study not only provide data
supporting the elucidation of CHS-induced hepatic metabolic disorders in fish but also offer insights for developing dietary
strategies to mitigate such damage in fish livers.
Key words: Micropterus salmoides; chronic heat stress; glycolipid metabolism; mitochondrial homeostasis; transcriptome
sequencing
Corresponding authors: LIU Yu. E-mail: nydxliuyu@163.com;
DENG Junming. E-mail: djunming@163.com

Funding projects: National Natural Science Foundation of China (32273152); Level Talent Startup Grant from Foshan Uni-
versity (CGZ07001)

https://www.china-fishery.cn 中国水产学会主办 sponsored by China Society of Fisheries
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