Transcriptome Sequencing Reveals High-Salt Diet-Induced Abnormal Liver Metabolic Pathways in Mice
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.
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Posted 13 Jan, 2021
Received 01 Mar, 2021
On 23 Feb, 2021
On 23 Feb, 2021
On 23 Feb, 2021
Invitations sent on 13 Jan, 2021
On 13 Jan, 2021
On 07 Jan, 2021
On 07 Jan, 2021
On 04 Jan, 2021
Transcriptome Sequencing Reveals High-Salt Diet-Induced Abnormal Liver Metabolic Pathways in Mice
Posted 13 Jan, 2021
Received 01 Mar, 2021
On 23 Feb, 2021
On 23 Feb, 2021
On 23 Feb, 2021
Invitations sent on 13 Jan, 2021
On 13 Jan, 2021
On 07 Jan, 2021
On 07 Jan, 2021
On 04 Jan, 2021
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