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A novel chicken model of fatty liver disease induced by high cholesterol and low choline diets

机译:高胆固醇和低胆碱饮食诱导的脂肪肝病新型鸡模型

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摘要

Fatty liver diseases, common metabolic diseases in chickens, can lead to a decrease in egg production and sudden death of chickens. To solve problems caused by the diseases, reliable chicken models of fatty liver disease are required. To generate chicken models of fatty liver, 7-week-old ISA female chickens were fed with a control diet (17% protein, 5.3% fat, and 1,300 mg/kg choline), a low protein and high fat diet (LPHF, 13% protein, 9.1% fat, and 1,300 mg/kg choline), a high cholesterol with low choline diet (CLC, 17% protein, 7.6% fat with additional 2% cholesterol, and 800 mg/kg choline), a low protein, high fat, high cholesterol, and low choline diet (LPHFCLC, 13% protein, 12.6% fat with additional 2% cholesterol, and 800 mg/kg choline) for 4 wk. Our data showed that the CLC and LPHFCLC diets induced hyperlipidemia. Histological examination and the content of hepatic lipids indicated that the CLC and LPHFCLC diets induced hepatic steatosis. Plasma dipeptidyl peptidase 4, a biomarker of fatty liver diseases in laying hens, increased in chickens fed with the CLC or LPHFCLC diets. Hepatic ballooning and immune infiltration were observed in these livers accompanied by elevated interleukin 1 beta and lipopolysaccharide induced tumor necrosis factor mRNAs suggesting that the CLC and LPHFCLC diets also caused steatohepatitis in these livers. These diets also induced hepatic steatosis in Plymouth Rock chickens. Thus, the CLC and LPHFCLC diets can be used to generate models for fatty liver diseases in different strains of chickens. In ISA chickens fed with the CLC diet, peroxisome proliferator-activated receptor γ, sterol regulatory element binding transcription factor 1, and fatty acid synthase mRNAs increased in the livers, suggesting that lipogenesis was enhanced by the CLC treatment. Our data show that treatment with CLC or LPHFCLC for 4 wk induces fatty liver disease in chickens. These diets can be utilized to rapidly generate chicken models for fatty liver research.
机译:脂肪肝病,鸡群中常见的代谢疾病,可以导致鸡蛋产生的降低和鸡蝇猝死。为了解决疾病造成的问题,需要可靠的脂肪肝疾病的鸡肉模型。为了产生脂肪肝的鸡型,7周龄ISA雌性鸡用对照饮食(17%蛋白,5.3%脂肪和1,300 mg / kg胆碱),低蛋白质和高脂饮食(LPHF,13 %蛋白质,9.1%脂肪和1,300mg / kg胆碱),一种高胆碱饮食的高胆固醇(CLC,17%蛋白,7.6%脂肪,含有2%胆固醇,800毫克/ kg胆碱),低蛋白质,高脂肪,高胆固醇和低胆碱饮食(LPHFCLC,13%蛋白,12.6%脂肪,额外的2%胆固醇和800mg / kg胆碱)4周。我们的数据显示CLC和LPHFCLC饮食诱导高脂血症。组织学检查和肝脂质的含量表明,CLC和LPHCCLC饮食诱发肝脏脂肪变性。血浆二肽基肽酶4是饲养母鸡脂肪肝疾病的生物标志物,随着CLC或LPHFCLC饮食喂养的鸡中增加。在这些肝脏中观察到肝脏膨胀和免疫渗透,伴随着白细胞介素1β和脂多糖诱导的肿瘤坏死因子MRNA,表明CLC和LPHCCCLC饮食也导致这些肝脏的脱脂性。这些饮食也诱导普利茅斯岩鸡的肝脏脂肪变性。因此,CLC和LPHFCLC饮食可用于生成不同鸡脂肪肝疾病的模型。在患有CLC饮食的ISA鸡中,过氧化物体增殖物激活的受体γ,甾醇调节元素结合转录因子1和脂肪酸合酶MRNA在肝脏中增加,表明CLC处理提高了脂肪生成。我们的数据显示,用CLC或LPHFCLC治疗4周的治疗鸡肉中的脂肪肝疾病。这些饮食可用于迅速生成脂肪肝研究的鸡型。

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