Open AccessEndogenously increased n-3 PUFA levels in fat-1 transgenic mice do not protect from non-alcoholic steatohepatitis
Author(s) -
Marie Liebig,
Dirk Dannenberger,
Brigitte Vollmar,
Kerstin Abshagen
Publication year - 2019
Publication title -
hepatobiliary surgery and nutrition
Language(s) - English
Resource type - Journals
eISSN - 2304-389X
pISSN - 2304-3881
DOI - 10.21037/hbsn.2019.04.03
Subject(s) - steatohepatitis , fatty liver , steatosis , polyunsaturated fatty acid , medicine , endocrinology , cd36 , genetically modified mouse , transgene , fibrosis , adipose tissue , fatty acid , biology , disease , biochemistry , receptor , gene
Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease worldwide, ranging from simple steatosis to non-alcoholic steatohepatitis (NASH) and fibrosis. Possible reasons for the NAFLD epidemic in industrialized countries are the high intake of pro-inflammatory n-6 polyunsaturated fatty acids (n-6 PUFAs) and low consumption of healthy n-3 PUFAs. Due to their anti-inflammatory properties, n-3 PUFAs may have the potential to alleviate chronic liver disease. Herein, we examined the therapeutic effect of increased n-3 PUFA tissue levels in fat-1 transgenic mice on progressive NASH.