期刊
AQUACULTURE
卷 540, 期 -, 页码 -出版社
ELSEVIER
DOI: 10.1016/j.aquaculture.2021.736691
关键词
Muscle; Cold stress; MAPK signaling pathway; Lipidomics; Aquaculture; Takifugu fasciatus
资金
- National Key R&D Program of China [2018YFD0900301]
- National Natural Science Foundation of China [31800436]
- Natural Science Foundation(NSF) of Jiangsu Province of China [BK20180728]
- Postgraduate Research & Practice Innovation Program of Jiangsu Province [KYCX20_1262]
This study investigated the impact of low temperature on the skeletal muscle of T. fasciatus, revealing that it damages muscle microstructure, upregulates antioxidant enzyme activities, and regulates specific signaling pathways and lipid metabolism pathways.
Low temperature is an important environmental factor affecting the breeding industry. Due to sudden cold waves or seasonal changes, huge losses have been caused to the breeding industry all over the world. We investigated the effect of temperature gradient (25, 19, and 13 C) and time (0, 6, 24, and 96 h) on the histomorphology, antioxidant enzyme activity, mitogen-activated protein kinase pathway, and lipidomics of the skeletal muscle from T. fasciatus. The results showed that low temperature damaged muscle microstructure and caused antioxidant enzyme activities (superoxide dismutase, glutathione peroxidase and catalase) upregulation. The mitogenactivated protein kinase (MAPK), including extracellular regulated protein kinases (ERK), c-Jun N-terminal kinase (JNK), and p38MAPK, was upregulated under cold stress. The expression of genes involved in lipogenesis [6-phosphate glucose dehydrogenase, glucose-6-phosphate dehydrogenase, fatty acid synthase, acetyl-coacarboxylase, lipoprteinlipase, sterol-regulatory element binding protein-1], lipolysis [hormone-sensitive lipase, and carnitine palmitoyltransferase-1], and transcription [peroxisome proliferator-activated receptor alpha, peroxisome proliferator-activated receptor gamma] were upregulated. Lipidomics results showed that phospholipid metabolites increased under cold stress, which compensated for the integrity of cell membranes. Overall, this study showed that T. fasciatus may adjust fat metabolism through MAPK to compensate for cell membrane damage in muscles caused by low temperature. Our results reveal the possibility that phospholipid metabolites can be used as potential feeds, and further reveal the mechanism of resistance to low temperatures.
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