转录组
生物
代谢物
内科学
内分泌学
代谢组学
脂质代谢
花生四烯酸
甘油三酯
脂肪酸
棕榈酸
新陈代谢
油酸
基因
基因表达
生物化学
胆固醇
酶
生物信息学
医学
作者
Rong Luo,C. Chen,Yuan Shi,Tao Qing,Ding-Ping Bai,A. Li
标识
DOI:10.1080/00071668.2022.2154638
摘要
1. In this study, transcriptomics and metabolomics were used to analyse changes in gene expression and metabolites in the liver of 70-d-old mule ducks after 10 and 20 d of continuous overfeeding.2. In the free-feeding group, 995 differentially expressed genes and 51 metabolites (VIP >1, P < 0.05) were detected in the early stage, and 3,448 differentially expressed genes and 55 metabolites (VIP >1, P < 0.05) were detected in the later stage. There were 775 differentially expressed genes and 47 metabolites (VIP >1, P < 0.05) detected in the early stage of the overfeeding group, and 6,719 differentially expressed genes and 57 metabolites (VIP >1, P < 0.05) detected in the later stage.3. There were no significant differences between the early stage in the overfeeding and free-feeding groups at the transcriptional and metabolic levels. Oleic acid and palmitic acid synthesis increased in the early stage of the overfeeding and free-feeding groups, however, these were inhibited in the late stage. Fatty acid oxidation and β-oxidation pathways were inhibited and insulin resistance was enhanced significantly in the late overfeeding stage.4. In the early stage, the digestion and absorption of fat in the overfeeding and free-feeding groups were enhanced. In the later stage, the ability to store triglyceride in the overfeeding group was greater than in the free-feeding group.5. The expression of nuclear factor κB (NFκB), a key inflammatory factor, was inhibited in the late stage of overfeeding, while arachidonic acid (AA), a metabolite with anti-inflammatory properties, increased in the late stage of overfeeding to inhibit the inflammatory effects caused by excessive lipid accumulation. These results add to the understanding of the mechanism of production of fatty liver in mule ducks and facilitate the development of treatments for non-alcoholic fatty liver disease.
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