Although salt plays an important role in maintaining the normal physiological metabolism of the human body, many abnormalities in the liver caused by a high-salt diet, especially with normal pathological results, are not well characterized. Eight-week-old female C57BL/6 mice were randomly divided into a normal group and a high salt group. These groups were then fed with normal or sodium-rich chow (containing 6% NaCl) for 6 weeks. Liver injury was evaluated, and the influences of a high-salt diet on the liver were analyzed by transcriptome sequencing at the end of week 6. We found that although no liver parenchymal injury could be 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 enzymatic 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 numerous biological functions, were involved in liver dysfunction due to a high-salt diet. This included some known pathways and many novel ones, such as retinol metabolism, linoleic acid metabolism, steroid hormone biosynthesis, and signaling pathways. A high-salt diet can induce serious abnormal liver metabolic activities in mice at the transcriptional level, although substantial physical damage may not yet be visible. This study, to our knowledge, was 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. This study also provides a serious candidate direction for further research on the physiological impacts of high-salt diets.

中文翻译：

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转录组测序揭示高盐饮食诱导小鼠肝脏代谢途径异常

虽然盐对维持人体正常的生理代谢具有重要作用，但高盐饮食引起的肝脏的许多异常，尤其是病理结果正常，尚未得到很好的表征。8周龄雌性C57BL/6小鼠随机分为正常组和高盐组。然后给这些组喂食正常或富含钠的食物（含 6% NaCl）6 周。评估肝损伤，并在第 6 周结束时通过转录组测序分析高盐饮食对肝脏的影响。我们发现，虽然高盐喂养后未发现肝实质损伤，但许多代谢异常已根据转录组测序结果形成。差异表达基因的 GO 和 KEGG 富集分析表明，至少 15 种酶活性和多种物质的代谢受到高盐饮食的影响。此外，高盐饮食导致的肝功能障碍涉及多种信号传导和代谢途径，以及多种生物学功能。这包括一些已知的通路和许多新通路，如视黄醇代谢、亚油酸代谢、类固醇激素生物合成和信号通路。高盐饮食会在转录水平上诱导小鼠肝脏代谢活动的严重异常，尽管实质性的物理损伤可能尚未显现。据我们所知，这项研究首次在组学水平上揭示了高盐饮食对肝脏的影响，并为潜在的临床风险评估、致病机制和对抗肝功能障碍的药物设计提供理论支持。这项研究还为进一步研究高盐饮食的生理影响提供了一个重要的候选方向。