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

Alcoholic fatty liver is the earliest stage of alcohol-induced liver disease leading to liver cirrhosis. beta-Conglycinin, one of the soy proteins, is known to prevent non-alcoholic fatty liver, hyperlipidemia and obesity. Therefore, we examined whether beta-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% beta-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) gamma 2, a nuclear transcription factor known for regulating lipid metabolism and de novo lipogenesis. The liver TG of ethanol-administered beta-conglycinin-fed mice was significantly lower than that in those fed casein, although ethanol increased the amount of liver TG in mice fed beta-conglycinin. The increased levels of PPAR gamma 2 protein and its target gene CD36 in response to an ethanol were not observed in mice fed beta-conglycinin. Moreover, beta-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 beta-conglycinin-fed mice than in the casein-fed mice. In conclusion, beta-conglycinin supplementation appears to prevent the development of fatty liver in mice caused by ethanol consumption via the suppression of alcohol induced activation of PPAR gamma 2 and the downregulation of the basal expression of de novo lipogenesis. (C) 2017 Elsevier Inc. All rights reserved.