脂质代谢
氧化应激
过氧化物酶体增殖物激活受体
生物
抗氧化剂
脂质过氧化
脂质氧化
脂滴
生物化学
代谢组
内科学
内分泌学
化学
受体
医学
代谢物
作者
Miaomiao Xue,Pao Xu,Wen Huang,Jianxiang Chen,Qingyong Wang,Jun He,Cijiang He,Chun-Yan Kong,Changyou Song,Hongxia Li
出处
期刊:Antioxidants
[MDPI AG]
日期:2023-08-15
卷期号:12 (8): 1615-1615
被引量:1
标识
DOI:10.3390/antiox12081615
摘要
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.
科研通智能强力驱动
Strongly Powered by AbleSci AI