Dietary β-conglycinin prevents acute ethanol-induced fatty liver in mice

脂肪生成 内分泌学 内科学 脂肪肝 脂肪变性 酒精性脂肪肝 酒精性肝病 乙醇 高脂血症 肝损伤 脂质代谢 CD36 化学 生物 肝硬化 生物化学 医学 受体 糖尿病 疾病
作者
Reina Ikaga,Dongyang Li,Tomomi Yamazaki
出处
期刊:Biochemical and Biophysical Research Communications [Elsevier BV]
卷期号:493 (1): 542-547 被引量:4
标识
DOI:10.1016/j.bbrc.2017.08.155
摘要

Alcoholic fatty liver is the earliest stage of alcohol-induced liver disease leading to liver cirrhosis. β-Conglycinin, one of the soy proteins, is known to prevent non-alcoholic fatty liver, hyperlipidemia and obesity. Therefore, we examined whether β-conglycinin feeding has an effect on the prevention of acute ethanol-induced fatty liver in mice. Male C57BL/6J mice were fed with 20 energy% β-conglycinin or casein for 4 weeks prior to ethanol administration and were then given ethanol or glucose, as a control, by gavage. Ethanol significantly increased liver triglyceride (TG) in mice fed casein due to the activation of peroxisome proliferator-activated receptor (PPAR) γ2, a nuclear transcription factor known for regulating lipid metabolism and de novo lipogenesis. The liver TG of ethanol-administered β-conglycinin-fed mice was significantly lower than that in those fed casein, although ethanol increased the amount of liver TG in mice fed β-conglycinin. The increased levels of PPARγ2 protein and its target gene CD36 in response to an ethanol were not observed in mice fed β-conglycinin. Moreover, β-conglycinin decreased the basal expression of de novo lipogenesis-related genes such as stearoyl-CoA desaturase-1, and therefore, the expressions of these genes were lower in the ethanol-administered β-conglycinin-fed mice than in the casein-fed mice. In conclusion, β-conglycinin supplementation appears to prevent the development of fatty liver in mice caused by ethanol consumption via the suppression of alcohol-induced activation of PPARγ2 and the downregulation of the basal expression of de novo lipogenesis.
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