Institute of Biotechnology, National Taiwan University, Taipei, Taiwan 10617; Department of Animal Science and Technology, National Taiwan University, Taipei, Taiwan 10617.
Department of Animal Science and Technology, National Taiwan University, Taipei, Taiwan 10617.
Poult Sci. 2021 Mar;100(3):100869. doi: 10.1016/j.psj.2020.11.046. Epub 2020 Nov 30.
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.
脂肪肝疾病是鸡的常见代谢疾病,可导致产蛋量下降和鸡突然死亡。为了解决这些疾病引起的问题,需要可靠的鸡脂肪肝模型。为了生成鸡脂肪肝模型,将 7 周龄 ISA 雌性鸡用对照饮食(17%蛋白质、5.3%脂肪和 1300mg/kg 胆碱)、低蛋白高脂肪饮食(LPHF,13%蛋白质、9.1%脂肪和 1300mg/kg 胆碱)、高胆固醇低胆碱饮食(CLC,17%蛋白质、7.6%脂肪外加 2%胆固醇和 800mg/kg 胆碱)、低蛋白、高脂肪、高胆固醇和低胆碱饮食(LPHFCLC,13%蛋白质、12.6%脂肪外加 2%胆固醇和 800mg/kg 胆碱)喂养 4 周。我们的数据表明,CLC 和 LPHFCLC 饮食诱导了高脂血症。组织学检查和肝脂质含量表明,CLC 和 LPHFCLC 饮食诱导了肝脂肪变性。血浆二肽基肽酶 4,一种产蛋母鸡脂肪肝的生物标志物,在饲喂 CLC 或 LPHFCLC 饮食的鸡中增加。在这些肝脏中观察到肝气球样变和免疫浸润,同时伴随着白细胞介素 1β和脂多糖诱导的肿瘤坏死因子 mRNA 的升高,表明 CLC 和 LPHFCLC 饮食也导致了这些肝脏的脂肪性肝炎。这些饮食还在波美拉尼亚鸡中诱导了肝脂肪变性。因此,CLC 和 LPHFCLC 饮食可用于生成不同品种鸡脂肪肝模型。在饲喂 CLC 饮食的 ISA 鸡中,肝脏中过氧化物酶体增殖物激活受体 γ、固醇调节元件结合转录因子 1 和脂肪酸合酶 mRNA 增加,表明 CLC 处理增强了脂肪生成。我们的数据表明,用 CLC 或 LPHFCLC 处理 4 周会导致鸡发生脂肪肝疾病。这些饮食可用于快速生成鸡脂肪肝研究模型。