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Data_Sheet_1_Hepatic Injury Induced by Dietary Energy Level via Lipid Accumulation and Changed Metabolites in Growing Semi-Fine Wool Sheep.docx

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frontiersin.figshare.com2023-06-06 更新2025-03-22 收录
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https://frontiersin.figshare.com/articles/dataset/Data_Sheet_1_Hepatic_Injury_Induced_by_Dietary_Energy_Level_via_Lipid_Accumulation_and_Changed_Metabolites_in_Growing_Semi-Fine_Wool_Sheep_docx/16664761/1
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Liver injury threatens the overall health of an organism, as it is the core organ of the animal body. Liver metabolism is affected by numerous factors, with dietary energy level being a crucial one. Therefore, the present study aimed to evaluate hepatic injury and to describe its metabolic mechanism in ruminants fed diets with different dietary energy levels. A total of 25 Yunnan semi-fine wool sheep were fed diets with five dietary metabolic energy levels and were randomly assigned to five groups as follows: low energy (LE), medium–low energy (MLE), medium energy (ME), medium–high energy (MHE), and high energy (HE). The results revealed that the average optical density (AOD) of lipid droplets in the LE, MLE, and HE groups was higher than that in the ME and MHE groups. The enzyme activity of alanine aminotransferase (ALT) was the lowest in the ME group. An increase in dietary energy level promoted the superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px) activity and altered the malondialdehyde (MDA) and protein carbonyl (PCO) concentration quadratically. In addition, both high and low dietary energy levels upregulated the mRNA abundance of proinflammatory cytokine interleukin (IL)-1β, nuclear factor-kappa B (NF-κB), and tumor necrosis factor (TNF)-α. Metabonomic analysis revealed that 142, 77, 65, and 108 differential metabolites were detected in the LE, MLE, MHE, and HE groups, compared with ME group respectively. These metabolites were involved in various biochemical pathways, such as glycolipid, bile acid, and lipid metabolism. In conclusion, both high and low dietary energy levels caused hepatic injury. Section staining and metabonomic results revealed that hepatic injury might be caused by altered metabolism and lipid accumulation induced by lipid mobilization.

肝脏损伤对生物体的整体健康构成威胁,因其乃动物体内之核心器官。肝脏代谢受诸多因素影响,其中膳食能量水平尤为关键。鉴于此,本研究旨在评估肝损伤并描述其在不同膳食能量水平饲养的反刍动物中的代谢机制。共选取25只云南半细毛羊,分别喂食五种不同膳食代谢能量水平的饲料,并将它们随机分为五组,具体如下:低能量组(LE)、中低能量组(MLE)、中等能量组(ME)、中高能量组(MHE)和高能量组(HE)。结果显示,LE、MLE和HE组的脂滴平均光密度(AOD)高于ME和MHE组。丙氨酸转氨酶(ALT)的酶活性在ME组最低。膳食能量水平的增加促进了超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶(GSH-Px)的活性,并二次改变了丙二醛(MDA)和蛋白质羰基(PCO)的浓度。此外,高能量和低能量膳食水平均上调了促炎细胞因子白细胞介素(IL)-1β、核因子κB(NF-κB)和肿瘤坏死因子(TNF)-α的mRNA丰度。代谢组学分析显示,与ME组相比,LE、MLE、MHE和HE组分别检测到142、77、65和108种差异代谢物。这些代谢物涉及多种生化途径,如糖脂、胆汁酸和脂质代谢。总之,高能量和低能量膳食水平均导致肝损伤。切片染色和代谢组学结果揭示了肝脏损伤可能由代谢改变和由脂质动员引起的脂质积累所导致。
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