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Research Article
Kun Huang
Department of Gastroenterology, Civil Aviation General Hospital
Corresponding Author
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Although salt plays an important role in maintaining the normal physiological metabolism of the human body, many potential abnormalities in liver, especially with normal pathological results, caused by high-salt diet are not well characterized.
Methods: Eight-week-old female C57BL/6 mice were randomly divided into a normal group and a high salt group. After feeding with normal or sodium-rich chow (containing 6% NaCl) for 6 weeks. Liver injury were evaluated and the influences of a high-salt diet on liver were analyzed by transcriptome sequencing.
Results: We found that although no liver parenchymal injury was found after high-salt feeding, many metabolic abnormalities had formed based on transcriptome sequencing results. GO and KEGG enrichment analyses of differentially expressed genes revealed that at least 15 enzyme activities and the metabolism of multiple substances were affected by a high-salt diet. Moreover, a variety of signaling, and metabolic pathways, as well as biological functions, including some known pathways and many novel ones, such as retinol metabolism, linoleic acid metabolism, steroid hormone biosynthesis, and signaling pathways, were involved in liver dysfunction due to a high-salt diet.
Conclusions: High-salt diet could induce a serious abnormal liver metabolic pathway in mice, although substantial damage has not yet been shown. This study is the first to reveal the impact of a high-salt diet on the liver at the omics level, and provides theoretical support for potential clinical risk evaluation, pathogenic mechanisms, and drug design for combating liver dysfunction, and this study also provides a serious candidate direction for further research on the physiological impacts of high-salt diets.
Keywords
high-salt diet, transcriptome sequencing, liver
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CURRENT STATUS: Under Review
Version 1
Posted 13 Jan, 2021
No community comments so far
Editorial decision: Major revision
On 03 Jun, 2021
Reviews received
Received 01 Jun, 2021
Reviewers agreed
On 25 May, 2021
Reviewers agreed
On 20 May, 2021
Reviews received
Received 01 Mar, 2021
Reviewers agreed
On 23 Feb, 2021
Reviewers invited
Invitations sent on 13 Jan, 2021
Editor assigned
On 13 Jan, 2021
Editor invited
On 07 Jan, 2021
Submission checks complete
On 07 Jan, 2021
First submitted
On 04 Jan, 2021
Metrics
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Subject Areas
Gastroenterology & Hepatology
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This preprint is under consideration at BMC Gastroenterology. A preprint is a preliminary version of a manuscript that has not completed peer review at a journal. Research Square does not conduct peer review prior to posting preprints. The posting of a preprint on this server should not be interpreted as an endorsement of its validity or suitability for dissemination as established information or for guiding clinical practice.
Learn more about In Review
Research Article
Kun Huang
Department of Gastroenterology, Civil Aviation General Hospital
Corresponding Author
Badges
Prescreen
This manuscript passed our Prescreen assessment
Complete author information
Appropriate declaration statements
Potential risks to human health
Prescreen
Peer Review Timeline
CURRENT STATUS: Under Review
Version 1
Posted 13 Jan, 2021
No community comments so far
Editorial decision: Major revision
On 03 Jun, 2021
Reviews received
Received 01 Jun, 2021
Reviewers agreed
On 25 May, 2021
Reviewers agreed
On 20 May, 2021
Reviews received
Received 01 Mar, 2021
Reviewers agreed
On 23 Feb, 2021
Reviewers invited
Invitations sent on 13 Jan, 2021
Editor assigned
On 13 Jan, 2021
Editor invited
On 07 Jan, 2021
Submission checks complete
On 07 Jan, 2021
First submitted
On 04 Jan, 2021
Metrics
Comments: 0
PDF Downloads: ...
HTML Views: ...
Subject Areas
Gastroenterology & Hepatology
License:
This work is licensed under a CC BY 4.0 License. Read Full License
Background: Although salt plays an important role in maintaining the normal physiological metabolism of the human body, many potential abnormalities in liver, especially with normal pathological results, caused by high-salt diet are not well characterized.
Methods: Eight-week-old female C57BL/6 mice were randomly divided into a normal group and a high salt group. After feeding with normal or sodium-rich chow (containing 6% NaCl) for 6 weeks. Liver injury were evaluated and the influences of a high-salt diet on liver were analyzed by transcriptome sequencing.
Results: We found that although no liver parenchymal injury was found after high-salt feeding, many metabolic abnormalities had formed based on transcriptome sequencing results. GO and KEGG enrichment analyses of differentially expressed genes revealed that at least 15 enzyme activities and the metabolism of multiple substances were affected by a high-salt diet. Moreover, a variety of signaling, and metabolic pathways, as well as biological functions, including some known pathways and many novel ones, such as retinol metabolism, linoleic acid metabolism, steroid hormone biosynthesis, and signaling pathways, were involved in liver dysfunction due to a high-salt diet.
Conclusions: High-salt diet could induce a serious abnormal liver metabolic pathway in mice, although substantial damage has not yet been shown. This study is the first to reveal the impact of a high-salt diet on the liver at the omics level, and provides theoretical support for potential clinical risk evaluation, pathogenic mechanisms, and drug design for combating liver dysfunction, and this study also provides a serious candidate direction for further research on the physiological impacts of high-salt diets.
Figure 1
Figure 2
Figure 3
Figure 4
Figure 5
This is a list of supplementary files associated with this preprint. Click to download.
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