Alcohol is a globally well-established cause of fatty liver disease (FLD). Increased salt consumption is associated with an increased prevalence of adipocyte hypertrophy and liver injury. In this study, high dietary salt potentiated chronic alcohol-induced hepatic damage. We explored the physiological mechanism of alcoholic FLD in the gastrointestinal tract. Male C57BL/6J mice (8-week-old) were fed a high-salt diet (HSD; 4% NaCl) with or without chronic ethanol (CE) for 1 month. The fecal microbiota, serum biochemical indices, intestinal permeability, level of liver damage, and liver mitochondria were evaluated. The HSD, CE, and their combination (HSDE) significantly changed the gut microbiota's structure, and the HSDE mice contained more probiotic species (e.g., Bifidobacterium and Lactobacillus). The serum aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase levels were increased, and the lipid was accumulated in the liver tissues in the CE, HSD, and HSDE groups, which indicated liver damage, especially in the HSDE group. The increased intestinal permeability and mitochondrial dysfunction in the liver cells caused greater injury in the HSDE group than in the other groups. Thus, consuming HSD with alcohol contributes to FLD development and progression.

中文翻译：

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长期饮酒和高盐摄入可导致小鼠肠道菌群改变和肝脂肪变性。

酒精是脂肪肝疾病（FLD）的全球公认原因。食盐增加与脂肪细胞肥大和肝损伤的患病率增加有关。在这项研究中，高盐饮食增强了慢性酒精引起的肝损害。我们探讨了酒精性FLD在胃肠道中的生理机制。给雄性C57BL / 6J小鼠（8周龄）喂食高盐饮食（HSD； 4％NaCl），含或不含慢性乙醇（CE），持续1个月。评估粪便微生物群，血清生化指标，肠通透性，肝损伤水平和肝线粒体。HSD，CE及其组合（HSDE）显着改变了肠道菌群的结构，HSDE小鼠含有更多的益生菌物种（例如双歧杆菌和乳杆菌）。血清天冬氨酸转氨酶 CE，HSD和HSDE组的丙氨酸氨基转移酶和碱性磷酸酶水平升高，脂质积聚在肝组织中，这表明肝脏受损，尤其是HSDE组。肝细胞中肠道通透性的增加和线粒体功能障碍导致HSDE组的损伤比其他组更大。因此，与酒精一起食用HSD有助于FLD的发展和进程。