Endogenously increased n-3 PUFA levels in fat-1 transgenic mice do not protect from non-alcoholic steatohepatitis | Zendy

Marie Liebig | Zendy; Dirk Dannenberger | Zendy; Brigitte Vollmar | Zendy; Kerstin Abshagen | Zendy

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Endogenously 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.

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