Abstract

High-salt diet has been considered to cause health problems, but it is still less known how high-salt diet affects gut microbiota, protein digestion, and passage in the digestive tract. In this study, C57BL/6J mice were fed low- or high-salt diets (0.25 vs. 3.15% NaCl) for 8 weeks, and then gut contents and feces were collected. Fecal microbiota was identified by sequencing the V4 region of 16S ribosomal RNA gene. Proteins and digested products of duodenal, jejunal, cecal, and colonic contents were identified by LC-MS-MS. The results indicated that the high-salt diet increased Firmicutes/Bacteroidetes ratio, the abundances of genera Lachnospiraceae and Ruminococcus (P < 0.05), but decreased the abundance of Lactobacillus (P < 0.05). LC-MS-MS revealed a dynamic change of proteins from the diet, host, and gut microbiota alongside the digestive tract. For dietary proteins, high-salt diet seemed not influence its protein digestion and absorption. For host proteins, 20 proteins of lower abundance were identified in the high-salt diet group in duodenal contents, which were involved in digestive enzymes and pancreatic secretion. However, no significant differentially expressed proteins were detected in jejunal, cecal, and colonic contents. For bacterial proteins, proteins secreted by gut microbiota were involved in energy metabolism, sodium transport, and protein folding. Five proteins (cytidylate kinase, trigger factor, 6-phosphogluconate dehydrogenase, transporter, and undecaprenyl-diphosphatase) had a higher abundance in the high-salt diet group than those in the low-salt group, while two proteins (acetylglutamate kinase and PBSX phage manganese-containing catalase) were over-expressed in the low-salt diet group than in the high-salt group. Consequently, high-salt diet may alter the composition of gut microbiota and has a certain impact on protein digestion.

Highlights

  • Epidemiological evidence suggested that the intake of salt, especially sodium chloride, may increase the risk of non-communicable diseases such as hypertension, stroke, and other cardiovascular diseases (Meneton et al, 2005; He and MacGregor, 2009; Strazzullo et al, 2009; Mugavero et al, 2014; Millen et al, 2016)

  • A study indicated that high-salt diet increased the vulnerability to colitis, which was independent of Th17 cells pathway but associated with shifts in gut microbiota

  • A significant decrease in the genus Providencia and Proteus was detected in feces, indicating that high-salt diet played an important role in shaping gut microbiota during the feeding of sows (Trawnska et al, 2013)

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Summary

Introduction

Epidemiological evidence suggested that the intake of salt, especially sodium chloride, may increase the risk of non-communicable diseases such as hypertension, stroke, and other cardiovascular diseases (Meneton et al, 2005; He and MacGregor, 2009; Strazzullo et al, 2009; Mugavero et al, 2014; Millen et al, 2016). Animal studies declared that high-salt diet was regarded to have an adverse effect on gut health, by causing aggravation of tissue inflammation and autoimmune diseases (Yi et al, 2015). Few data are available on the effect of high-salt diet on gut microbiota. A study indicated that high-salt diet increased the vulnerability to colitis, which was independent of Th17 cells pathway but associated with shifts in gut microbiota. A significant decrease in the genus Providencia and Proteus was detected in feces, indicating that high-salt diet played an important role in shaping gut microbiota during the feeding of sows (Trawnska et al, 2013). A salt-tolerant gene which belongs to Bacteroides has been proven to avoid the influence of high salt (Culligan et al, 2014), which seems to explain that highsalt diet may induce high proliferation of certain gut microbiota

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