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首页> 外文期刊>Scientific reports. >Insulin resistance and metabonomics analysis of fatty liver haemorrhagic syndrome in laying hens induced by a high-energy low-protein diet
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Insulin resistance and metabonomics analysis of fatty liver haemorrhagic syndrome in laying hens induced by a high-energy low-protein diet

机译:脂肪肝血液综合征在高能量低蛋白饮食诱导母鸡中的胰岛素抵抗及代谢综合征

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Fatty liver haemorrhagic syndrome (FLHS) is a widespread metabolic disease in laying hens that causes a decrease in egg production and even death. Insulin resistance is a major contributor to the pathogenesis of nonalcoholic fatty liver disease. However, the relationship between FLHS and the insulin resistance mechanisms underlying FLHS is not well elucidated. Therefore, we established an FLHS model induced by feeding a high-energy low-protein diet. In the current study, we found that the fasting glucose and insulin concentrations were elevated in the FLHS group compared with the control group during the experimental period. The results of the oral glucose tolerance test (OGTT) and insulin sensitivity test (IST) showed a high level of insulin resistance in the FLHS model. InsR, 4EBP-1, Glut-1 and Glut-3 mRNA expression were decreased, and TOR, S6K1, and FOXO1 were elevated (P??0.05). Metabolomic analysis with GC/MS identified 46 differentially expressed metabolites between these two groups, and of these, 14 kinds of metabolism molecules and 32 kinds of small metabolism molecules were decreased (P??0.05). Further investigation showed that glucose, lipid and amino acid metabolism blocks in?the progression of FLHS by GO functional and pathway analysis. Overall, these results suggest that insulin resistance participated in FLHS; comprehensively, metabolites participated in the dysregulated biological process.
机译:脂肪肝脏出血性综合征(FLHS)是铺设母鸡的广泛代谢疾病,导致鸡蛋产生甚至死亡。胰岛素抵抗是非酒精性脂肪肝疾病发病机制的主要因素。然而,FLHS与胰岛素抵抗机制之间的关系并不熟悉。因此,我们建立了通过喂养高能低蛋白质饮食而引起的FLHS模型。在目前的研究中,我们发现在实验期间与对照组相比,在FLHS组中升高了空腹葡萄糖和胰岛素浓度。口服葡萄糖耐量试验(OGTT)和胰岛素敏感性试验(IST)的结果显示了FLHS模型中的高水平胰岛素抵抗力。 INSR,4EBP-1,凝胶-1和凝胶-3 mRNA表达减少,升高,S6K1和FOXO1升高(P≤0.05)。使用GC / MS的代谢组分析鉴定了这两组之间的46型差异表达代谢物,其中14种代谢分子和32种小型代谢分子减少(P?<?0.05)。进一步的研究表明,葡萄糖,脂质和氨基酸代谢嵌段α通过GO功能和途径分析进行FLHS的进展。总体而言,这些结果表明胰岛素抵抗参加了FLHS;全面地,代谢物参与了失调的生物过程。

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