Abstract
BackgroundIt 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.MethodsWe 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.ResultsHigh-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.ConclusionsWe 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.Electronic supplementary materialThe online version of this article (doi:10.1186/s12944-015-0002-9) contains supplementary material, which is available to authorized users.
Highlights
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 examined the effect of a high-salt and high-fat diet (HS/HFD) and HFD on liver damage in Tg/apoE KO (TgKO) mice
Effects of anti-oxidant, tempol, on nonalcoholic steatohepatitis (NASH) in HS/HFD-fed mice The present findings suggest that excessive salt intake could be accelerated the onset and progression of HFDinduced NASH due to reactive oxygen species (ROS) overproduction
Summary
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 facilitates the development of nonalcoholic steatohepatitis (NASH), which is frequently associated with metabolic syndrome. In the onset and progression of NASH, cholesterol plays a major role in development of NASH causing oxidative stress in hepatic tissue [13]. A high-fat diet (HFD) increases free fatty acids, which induce mitochondrial β oxidation and the overproduction of free radicals [13], both of which play an important role in progression of NASH. Given the experimental fact that vitamin E and C improved liver damage in NASH [14,15], environmental and intrinsic reactive oxygen species (ROS)-increasing stimuli accelerate the onset and progression of NASH
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