@article{oai:soar-ir.repo.nii.ac.jp:00020085,
 author = {Uetake, Y and Ikeda, H and Irie, R and Tejima, K and Matsui, H and Ogura, S and Wang, H and Mu, SY and Hirohama, D and Ando, K and Sawamura, T and Yatomi, Y and Fujita, T and Shimosawa, T},
 journal = {LIPIDS IN HEALTH AND DISEASE},
 month = {Feb},
 note = {Background: It is widely known that salt is an accelerating factor for the progression of metabolic syndrome and causes cardiovascular diseases, most likely due to its pro-oxidant properties. We hypothesized that excessive salt intake also facilitates the development of nonalcoholic steatohepatitis (NASH), which is frequently associated with metabolic syndrome.<br/>Methods: We examined the exacerbating effect of high-salt diet on high-fat diet-induced liver injury in a susceptible model to oxidative stress, apoE knockout and lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) transgenic mice.<br/>Results: High-salt diet led to NASH in high-fat diet-fed LOX-1 transgenic/apoE knockout mice without affecting high-fat diet-induced dyslipidemia or hepatic triglyceride accumulation. Additionally, a high-salt and high-fat diet stimulated oxidative stress production and inflammatory reaction to a greater extent than did a high-fat diet in the liver of LOX-1 transgenic/apoE knockout mice.<br/>Conclusions: We demonstrated that high-salt diet exacerbated NASH in high-fat diet-fed LOX-1 transgenic /apoE knockout mice and that this effect was associated with the stimulation of oxidative and inflammatory processes; this is the first study to suggest the important role of excessive salt intake in the development of NASH., Article, LIPIDS IN HEALTH AND DISEASE.14:6(2015)},
 title = {High-salt in addition to high-fat diet may enhance inflammation and fibrosis in liver steatosis induced by oxidative stress and dyslipidemia in mice},
 volume = {14},
 year = {2015}
}