High-salt in addition to high-fat diet may enhance inflammation and fibrosis in liver steatosis induced by oxidative stress and dyslipidemia in mice.

Abstract

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.

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.

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.

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.

• Authors: Yuzaburo Uetake, Hitoshi Ikeda, Rie Irie, Kazuaki Tejima, Hiromitsu Matsui, Sayoko Ogura, Hong Wang, ShengYu Mu, Daigoro Hirohama, Katsuyuki Ando, Tatsuya Sawamura, Yutaka Yatomi, Toshiro Fujita, Tatsuo Shimosawa
• Journal: Lipids in health and disease (Lipids Health Dis) Vol. 14 Pg. 6 (Feb 13 2015) ISSN: 1476-511X [Electronic] England
• PMID: 25888871 (Publication Type: Journal Article)

Chemical References

• Olr1 protein, mouse
• Scavenger Receptors, Class E
• Sodium, Dietary
• Superoxides
• NADP

Topics

• Animals
• Blotting, Western
• Diet, High-Fat (adverse effects)
• Dyslipidemias (complications, pathology)
• Fatty Liver (etiology, pathology)
• Fibrosis (etiology)
• Inflammation (etiology)
• Liver (chemistry, pathology)
• Male
• Mice
• Mice, Knockout
• NADP (metabolism)
• Oxidative Stress (drug effects, physiology)
• Reverse Transcriptase Polymerase Chain Reaction
• Scavenger Receptors, Class E (biosynthesis, genetics)
• Sodium, Dietary (adverse effects)
• Superoxides (analysis)