过氧化物酶体增殖物激活受体信号介导的 13-S-羟基十八碳烯酸参与淡水鼓 Aplodinotus grunniens 肝脏中的脂质代谢紊乱和氧化应激,Antioxidants

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过氧化物酶体增殖物激活受体信号介导的 13-S-羟基十八碳烯酸参与淡水鼓 Aplodinotus grunniens 肝脏中的脂质代谢紊乱和氧化应激
Antioxidants ( IF 6.0 ) Pub Date : 2023-08-15 , DOI: 10.3390/antiox12081615
Miaomiao Xue ₁ , Pao Xu _{1,

2} , Haibo Wen _{1,

2} , Jianxiang Chen _{1,

2} , Qingyong Wang ₁ , Jiyan He ₁ , Changchang He ₁ , Changxin Kong ₁ , Changyou Song _{1,

2} , Hongxia Li _{1,

2}

Affiliation

适当的膳食脂质水平对于水产动物的营养需求、快速生长和健康维持至关重要，而膳食脂质摄入过多会导致脂质沉积，影响鱼类健康。然而，淡水鼓（Aplodinotus grunniens）肝脏中脂质过度沉积的症状仍不清楚。本研究通过为期 4 个月的高脂饲料饲养实验和为期 6 周的饥饿应激实验来评估格鲁尼乌龟肝脏脂质沉积的生理变化和潜在机制。结果表明，高脂肪饮食引起的脂质沉积与条件因子（CF）、内脏指数（VSI）和肝体指数（HSI）增加有关。同时，脂质沉积导致生理代谢紊乱，抑制抗氧化能力，加重脂质代谢负担。脂质沉积促进脂肪酸合成但抑制分解代谢。具体来说，转录组和代谢组显示脂质代谢和抗氧化途径显着富集。此外，相互作用分析表明，过氧化物酶体增殖物激活受体（PPAR）介导的13-S-羟基十八烯酸（13（s）-HODE）可以作为调节脂质代谢和脂质沉积过程中氧化应激的关键靶标。 .格鲁尼恩斯。相反，通过脂质摄入限制实验，证实 PPAR 可以调节 A. grunniens 的脂质消耗和生理稳态。这些结果揭示了脂肪肝的分子基础，并为控制和预防脂肪肝提供了具体的分子靶点，这对于格鲁尼菌的可持续发展具有重要意义。

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Peroxisome Proliferator-Activated Receptor Signaling-Mediated 13-S-Hydroxyoctadecenoic Acid Is Involved in Lipid Metabolic Disorder and Oxidative Stress in the Liver of Freshwater Drum, Aplodinotus grunniens

The appropriate level of dietary lipids is essential for the nutrient requirements, rapid growth, and health maintenance of aquatic animals, while excessive dietary lipid intake will lead to lipid deposition and affect fish health. However, the symptoms of excessive lipid deposition in the liver of freshwater drums (Aplodinotus grunniens) remain unclear. In this study, a 4-month rearing experiment feeding with high-fat diets and a 6-week starvation stress experiment were conducted to evaluate the physiological alteration and underlying mechanism associated with lipid deposition in the liver of A. grunniens. From the results, high-fat-diet-induced lipid deposition was associated with increased condition factor (CF), viscerosomatic index (VSI), and hepatosomatic index (HSI). Meanwhile, lipid deposition led to physiological and metabolic disorders, inhibited antioxidant capacity, and exacerbated the burden of lipid metabolism. Lipid deposition promoted fatty acid synthesis but suppressed catabolism. Specifically, the transcriptome and metabolome showed significant enrichment of lipid metabolism and antioxidant pathways. In addition, the interaction analysis suggested that peroxisome proliferator-activated receptor (PPAR)-mediated 13-S-hydroxyoctadecenoic acid (13 (s)-HODE) could serve as the key target in regulating lipid metabolism and oxidative stress during lipid deposition in A. grunniens. Inversely, with a lipid intake restriction experiment, PPARs were confirmed to regulate lipid expenditure and physiological homeostasis in A. grunniens. These results uncover the molecular basis of and provide specific molecular targets for fatty liver control and prevention, which are of great importance for the sustainable development of A. grunniens.

更新日期：2023-08-15

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