Affiliation:
1. Kyoto Prefectural University of Medicine
2. Kyoto City Hospital
3. AiSTI Science CO., Ltd
Abstract
Abstract
Background
In this study, we investigated the mechanism by which excessive salt intake aggravates atherosclerosis by evaluating the changes in the gut microbiota, the expression of nutrient transporters in the gut, and the fatty acid composition in atherosclerosis.
Results
Sixteen-week-old male ApoE-deficient mice were either fed a high-fat, high-sucrose diet (HFHSD) or HFHSD, high-salt diet (HFHSD + 4%NaCl) for 8 weeks. The HFHSD + 4%NaCl group showed progression of atherosclerosis, and gut microbiota analysis revealed that this group had a reduced abundance of Allobaculum spp., Ruminococcaceae family, Lachnospiraceae family, and Alphaproteobacteria class compared to the HFHSD group. Furthermore, Cd36 gene expression levels were increased in the small intestine of the HFHSD + 4%NaCl group compared to those in the HFHSD group. The concentration of saturated fatty acids in serum and atherosclerotic lesions, was remarkably increased in the HFHSD + 4%NaCl group.
Conclusions
Dysbiosis induced by excessive salt intake increases the expression of long-chain fatty acid transporters in the intestinal tract, which increases the influx of saturated fatty acids into the body.
Publisher
Research Square Platform LLC
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