A high fat diet temporarily renders Sod1-deficient mice resistant to an oxidative insult
Patients with non-alcoholic fatty liver disease (NAFLD) may subsequently develop non-alcoholic steatohepatitis (NASH) after suffering from a second insult, such as oxidative stress. Aim of this study was to investigate the pathogenesis of the liver injury caused when lipids accumulate under conditions of intrinsic oxidative stress using mice that are deficient in superoxide dismutase 1 (SOD1) and the leptin receptor (Lepr). We established Sod1 −/−::Leprdb/db mice and carried out analyses of four groups of genetically modified mice, namely, wild type, Sod1−/−, Leprdb/db, and Sod1−/−::Leprdb/db mice.
Source: The Journal of Nutritional Biochemistry - Category: Biochemistry Authors: Junitsu Ito, Naoki Ishii, Ryusuke Akihara, Jaeyong Lee, Toshihiro Kurahashi, Takujiro Homma, Ryo Kawasaki, Junichi Fujii Source Type: research
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