Dietary ß-conglycinin prevents acute ethanol-induced fatty liver in mice.
Biochem Biophys Res Commun
; 493(1): 542-547, 2017 11 04.
Article
in En
| MEDLINE
| ID: mdl-28867186
ABSTRACT
Alcoholic fatty liver is the earliest stage of alcohol-induced liver disease leading to liver cirrhosis. ß-Conglycinin, one of the soy proteins, is known to prevent non-alcoholic fatty liver, hyperlipidemia and obesity. Therefore, we examined whether ß-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% ß-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 ß-conglycinin-fed mice was significantly lower than that in those fed casein, although ethanol increased the amount of liver TG in mice fed ß-conglycinin. The increased levels of PPARγ2 protein and its target gene CD36 in response to an ethanol were not observed in mice fed ß-conglycinin. Moreover, ß-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 ß-conglycinin-fed mice than in the casein-fed mice. In conclusion, ß-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.
Key words
Full text:
1
Collection:
01-internacional
Database:
MEDLINE
Main subject:
Soybean Proteins
/
Dietary Supplements
/
PPAR gamma
/
Antigens, Plant
/
Lipogenesis
/
Seed Storage Proteins
/
Globulins
/
Liver Diseases, Alcoholic
Type of study:
Etiology_studies
Limits:
Animals
Language:
En
Journal:
Biochem Biophys Res Commun
Year:
2017
Type:
Article
Affiliation country:
Japan