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Numerous studies have demonstrated that Cryptocaryon irritans can efficiently propagate in golden pompano (Trachinotus blochii), especially under intensive high-density culture, which can lead to large-scale infection, bacterial invasion, and major economic losses. By contrast, Siganus oramin is less susceptible to C. irritans infection. Here, we artificially infected S. oramin and T. blochii with C. irritans. We then used RNA-seq to characterize the expression of genes in the gills of S. oramin and T. blochii at different times after infection, conducted bioinformatics analysis of relevant pathways, and compared the differentially expressed genes in the two species. The aim of this study was to enhance our understanding of host-parasite interactions to aid the development of effective prevention and treatment strategies for C. irritans. Infection with C. irritans induced the differential expression of a large number of genes in the gills of S. oramin, indicating that S. oramin may respond to C. irritans infection by modifying the expression of genes at the transcriptional level. Our research showed that the Toll-like receptor signaling pathway, Antigen processing and presentation, Complement and coagulation cascades, and Cytosolic DNA-sensing pathway are involved in the immune response of S. oramin and T. blochii to C. irritans infection. However, T. blochii has a weak ability to mobilize neutrophils to participate in defense against C. irritans infection and differs from S. oramin in its ability to induce specific immune responses. Because of gill tissue damage during infection, dissolved oxygen intake is reduced, which increases physiological and metabolic stress. The metabolic pathways of S. oramin and T. blochii significantly differed; specifically, the main pathways in S. oramin were related to glucose and lipid metabolism, and the main pathways in T. blochii were related to amino acid metabolism. This may reduce the efficiency of ATP biosynthesis in T. blochii and result in dysfunctional energy metabolism. Therefore, differential immune and metabolic responses underlie differences in the resistance of S. oramin and T. blochii to C. irritans.

The golden pompano (Trachinotus blochii) is becoming increasingly popular among consumers for its delicate meat and high nutritional value. High farming density, eutrophication, and high-temperature conditions increase the probability of hypoxia and thus hypoxic stress, which poses a major challenge for the future development of golden pompano aquaculture. Here, we simulated severe hypoxic stress to distinguish hypoxia-tolerant and hypoxia-sensitive individuals from hundreds of fish. We then used next-generation sequencing to analyze the mRNA expression profiles of the brains and livers under hypoxia to identify the causes of differences in hypoxia tolerance among different groups. The pathways involved in highly expressed genes in the brain were mainly related to signal transduction, endocrine function, and environmental information processing, while the pathways involved in highly expressed genes in the liver were mainly related to metabolism. Under hypoxic conditions, the degradation of liver glycogen in the hypoxia-tolerant group was inhibited under hypoxia. However, in the hypoxia-intolerant group, glycogen decomposition is not inhibited, glucose consumption increases, and there is no tendency to convert to lipid metabolism, leading to metabolic disorders. In the process of adapting to hypoxia, fish first use anaerobic glycolysis to compensate for the lack of energy due to hypoxia. However, as the stress persists, glycolysis is inhibited, and lipid metabolism becomes the preferred mode of energy metabolism; specifically, acetyl-CoA may be produced through lipid metabolism in the hypoxia-tolerant group and then participate in the tricarboxylic acid cycle to provide energy. Death in the hypoxia-intolerant group may stem from the metabolic disorder of glucose and lipid homeostasis. Although additional research is needed to confirm these possibilities, our findings suggest that converting the preferred way of energy metabolism to lipid metabolism may be a way for fish to adapt to acute hypoxic stress.

With increased breeding density, the possibility of hypoxia increases. This study simulated the hypoxic environment (1.2 ± 0.2 mg / L) that may occur within 24 h of aquaculture to stress largemouth bass (Micropterus salmoides). The effects of this environment on related enzymes and genes were examined to explore the effects of hypoxia on lipid metabolism in the liver. Hypoxic stress increased liver triglyceride and non-esterified fatty acid content, and increased lipase (LPS) and lipoprotein lipase (LPL) activities related to fat mobilization. Hypoxia stress also significantly increased the expression levels of genes involved in fatty acid activation and fatty acid transport, including hormone-sensitive triglyceride lipase (HSL), solute carrier family member 27 member 6 (SLC27A6), peroxisomal proliferation activated receptor alpha (PPARA,) and acyl-CoA synthase long-chain family 4 (ACSL4). However, hypoxia stress significantly reduced the expression level of the carnitine palmitoyltransferase 1 (CPT-1) gene, with a downward trend of enzyme activity. The decreased level of CPT-1 was explained by negative regulation by miR-124 and miR-205, as measured by quantitative polymerase chain reaction and dual-luciferase reporter assays. Overall, acute hypoxic stress enhanced lipid mobilization, fatty acid activation, and fatty acid transport, but inhibited fatty acid oxidation by miR-124 and miR-205 down-regulation of CPT-1 expression. These findings provide new insights into the regulation of lipid metabolism in fish under hypoxic stress.

Increasing culture density have elevated the probability of hypoxia occurring, which will inevitably lead to hypoxia stress of fish. In the present study, we simulated a hypoxic environment (1.2 ± 0.2 mg/L) that is likely to occur during aquaculture for 24 h, and conducted an integrated analysis of miRNA-mRNA using high-throughput sequencing to reveal the regulatory role of miRNAs in the metabolism of largemouth bass (Micropterus salmoides) livers during acute hypoxia exposure. Based on the pathways implicated by the differentially expressed mRNA and differentially expressed miRNAs' target genes, 7 processes related to carbohydrate and lipid metabolism were identified, namely pyruvate metabolism, the insulin signaling pathway, fatty acid degradation, fatty acid biosynthesis, glycolysis / gluconeogenesis, the PPAR (peroxisome proliferators-activated receptors) signaling pathway, and the VEGF (vascular endothelial growth factor) signaling pathway. There were 13 differentially expressed miRNAs involved in glucose and lipid metabolism, including miR-130a-3p, miR-2188-5p, miR-15b-5p, miR-96-5p, miR-27a-3p, mIR-152-3p, miR-133-3p, miR-101b-3p, miR-221-3p, miR-222a-3p, miR-153-3p, miR-200b-3p and miR-142a-3p. Their target genes were acsl4, aldh3a, irs, ehhadh, bad, mknk1, pik3cb, minnp1, cyp7a1, hk1, pgm, and crk, respectively. Specifically, miRNAs play an important role in regulating glycolysis and lipid mobilization in fish under hypoxic conditions. According to our current and previous research results, we can speculate that miRNAs play an important regulatory role in the transformation of metabolic patterns under hypoxic conditions, and this regulatory role may be conservative. These results will be helpful to understand the hypoxic response mechanisms in fish.

Dissolved oxygen (DO) undountedly affects fish distribution, metabolism, and evern survival. Intensive aquaculture and environmental changes will inevitably lead to hypoxic stress for largemouth bass (Micropterus salmoides). The different metabolic responses and mechanism still remains relatively unknown during acute hypoxia exposure. In this study, largemouth bass were subjected to hypoxic stress (3.0 ± 0.2 mg/L and 1.2 ± 0.2 mg/L) for 24 h and 12 h reoxygenation to systemically evaluate indicators of glucose and lipid metabolism. A regulatory network was constructed using RNA-seq to further elucidate the transcriptional regulation of glucose and lipid metabolism. During hypoxia for 4 h, the liver glycogen, glucose and pyruvic acid contents significantly decreased, whereas plasma glucose content and liver lactic acid content increased significantly. The accumulation of liver triglycerides and non-esterified fatty acids was enhanced during hypoxia for 8 h. The activity of key enzymes revealed the different metabolic responses to hypoxia exposure for 4 h, including the enhancement of glycolysis, and inhibition of gluconeogenesis. Furthermore, hypoxia exposure for 8 h increased lipid mobilization, and inhibited the β-oxidation. In addition, an integrated regulatory network of 9 major pathways involved in the response to hypoxia exposure was constructed, including HIF signaling pathway, VEGF signaling pathway, AMPK signaling pathway, insulin signaling pathway and PPAR signaling pathway; glycolysis/gluconeogenesis, pyruvate metabolism, fatty acid degradation and fatty acid biosynthesis. Additionally, reoxygenation inhibited glycolysis, and promoted gluconeogenesis and lipid oxidation, but energy deficits persisted. In short, although the mobilization and activation of fatty acid in liver were enhanced in the early stage of hypoxia, glycolysis was the main energy source under acute hypoxia. The extent and duration of hypoxia determine the degree of change in energy metabolism.

Hypoxia is an adverse environmental condition for fish that can have multiple effects. Compared to the natural environment, high-density farming of Schizothorax prenanti is more likely to experience hypoxic conditions. To evaluate the effects of hypoxia, activities of enzymes and expressions of genes that are related to hypoxia responses were measured to understand lipid metabolism, antioxidant capacity, and immnue response changed during hypoxic conditions (dissolved oxygen: 3.0 ± 0.2 mg/L [MHG] and 1.2 ± 0.2 mg/L [SHG]). During hypoxia, the red blood cell content increased. Furthermore, the lactic acid levels in the brain, liver, and muscle increased. Surprisingly, brain Na+/K+-ATPase activity was decreased. Brain and muscle triglyceride (TG) increased at frst, and then decreased, while the nonesterified fatty acids (NEFA) opposite in the brain had the opposite response, Liver TG and NEFA increased during hypoxia. Brain lipoprotein lipase (LPL) activity decreased, but liver and muscle LPL activities and LPL mRNA levels increased during exposure at 0 h and 12 h. Fatty acid binding protein, fatty acid synthase, peroxisome proliferators activated receptor γ coactivator-1α, peroxisome proliferator activated receptors α and γ genes were up-regulated at different time points, especially in SHG. Also, in SHG, malondiadehyde (MDA) levels in the brain and Intestine increased to some extent. Total antioxidative capability (T-AOC) in the brain and muscle tissue decreased, while it increased in gill, Intestine and liver tissue. Catalase (CAT) activity in the brain, gill, Intestine and muscle increased, while it decreased in the liver. Glutathione peroxidase (GSH-Px) activity was decreased in all tissues except brain. The mRNA levels of superoxide dismutase, GSH-Px, CAT, and hypoxia-inducible factor 1 alpha in the brain, gill and liver increased during hypoxia. Tumor necrosis factor, interleukin 1 beta and tropinone reductase-like 22 levels were up-regulated in all tissues, especially in SHG. Also, brain, gill, liver and muscle HSP70 and HSP90 levels increased. In short, hypoxia enhanced lipid metabolism and antioxidant response, and induced up-regulation of antioxidant and immune genes to adapt to environmental hypoxic stress.

Temperature is a key factor that influences fish metabolism. Therefore, it is important to understand how temperature variation affects lipid metabolism and energy consumption in fish. We determined respiration frequency, Na