Premium
Endogenously elevated n‐3 polyunsaturated fatty acids alleviate acute ethanol‐induced liver steatosis
Author(s) -
Huang Wei,
Wang Bin,
Li Xiangyong,
Kang Jing X.
Publication year - 2015
Publication title -
biofactors
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.204
H-Index - 94
eISSN - 1872-8081
pISSN - 0951-6433
DOI - 10.1002/biof.1246
Subject(s) - steatosis , polyunsaturated fatty acid , ethanol , fatty liver , chemistry , steatohepatitis , medicine , food science , biochemistry , gastroenterology , fatty acid , disease
Effective means for the prevention of alcohol‐induced liver disease, a global health problem, have yet to be developed. We evaluated whether the high endogenous levels of omega‐3 polyunsaturated acids (n‐3 PUFA) in fat‐1 transgenic mice could protect them against acute ethanol‐induced liver steatosis. We induced alcoholic liver steatosis in 9‐week‐old male heterozygous fat‐1 mice and their wild‐type (WT) male littermates through three oral gavages of 60% ethanol at 4.7 g/kg body weight. Hepatic lipid accumulation was significantly increased in both alcohol treatment groups, but by much less in the fat‐1 group compared with the WT group. Fat‐1 mice exhibited significantly lower levels of total hepatic/plasma TG and plasma alanine aminotransferase activity. Accordingly, hepatic expression of lipogenesis‐related genes ( e.g ., SREBP‐1c, FAS, and SCD‐1) and plasma levels of inflammatory cytokines ( e.g ., IL‐6, TNF‐α, and MCP‐1) were reduced in the fat‐1 mice. Furthermore, decreased hepatic expression of cytochrome P450 2E1 (CYP2E1) and increased hepatic levels of PPAR‐α and HO‐1 were observed in the fat‐1 mice, compared to the WT mice. These findings show that elevated tissue n‐3 PUFA protect against acute ethanol‐induced liver steatosis in fat‐1 mice, possibly through the down‐regulation of hepatic lipogenesis, inflammatory response, and oxidative stress. © 2015 BioFactors, 41(6):453–462, 2015