Department of Nutritional Sciences, Molecular Nutritional Science, University of Vienna, Althanstraße 14 (UZA II), 1090, Vienna, Austria.
Institute of Nutritional Sciences, SD Model Systems of Molecular Nutrition, Friedrich-Schiller-University Jena, Dornburger Straße 22-25, 07743, Jena, Germany.
Eur J Nutr. 2020 Mar;59(2):787-799. doi: 10.1007/s00394-019-01945-2. Epub 2019 Mar 16.
Results of some epidemiological studies suggest that moderate alcohol consumption may be associated with a decreased risk to develop NAFLD. Here, the effect of the consumption of moderate beer and diluted ethanol, respectively, on the development of NAFLD were assessed.
Female C57BL/6J mice were fed a control diet (C-D) or a diet rich in fructose, fat and cholesterol (FFC) enriched isocalorically and isoalcoholically with beer (FFC + B) or plain ethanol (FFC + E) (2.5 g ethanol/kg body weight/day) for 7 weeks. Liver damage was assessed by histology using NAFLD activity score. Markers of inflammation, insulin resistance and adiponectin signaling were measured at mRNA and protein levels. Using J774A.1 cells as a model of Kupffer cells, the effect of alcoholic beverages on adiponectin receptor 1 (Adipor1) was assessed.
Hepatic triglyceride concentration, neutrophil granulocytes, iNOS protein concentrations and early signs of insulin resistance found in FFC-fed mice were significantly attenuated in FFC+ B-fed mice (P < 0.05 for all). These findings were associated with a super-induction of Adipor1 mRNA expression (+ ~ 18-fold compared to all other groups) and a decrease of markers of lipid peroxidation in liver tissue of FFC + B-fed mice when compared to FFC-fed animals. Similar differences were not found between FFC- and FFC+ E-fed mice. Expression of Adipor1 was also super-induced (7.5-fold) in J774A.1 cells treated with beer (equivalent to 2 mmol/L ethanol).
These data suggest that moderate intake of fermented alcoholic beverages such as beer at least partially attenuates NAFLD development through mechanisms associated with hepatic AdipoR1 expression.
一些流行病学研究的结果表明，适量饮酒可能与降低非酒精性脂肪性肝病（NAFLD）的发病风险有关。在此，评估了分别饮用适量啤酒和稀释乙醇对 NAFLD 发展的影响。
雌性 C57BL/6J 小鼠分别用对照饮食（C-D）或富含果糖、脂肪和胆固醇的饮食（FFC）喂养，并用啤酒（FFC + B）或普通乙醇（FFC + E）等热量和等酒精含量进行营养补充（每天 2.5 g 乙醇/公斤体重），共喂养 7 周。采用 NAFLD 活性评分评估肝损伤程度。用 mRNA 和蛋白质水平测量炎症、胰岛素抵抗和脂联素信号的标志物。用 J774A.1 细胞作为枯否细胞的模型，评估酒精饮料对脂联素受体 1（Adipor1）的影响。
FFC 喂养的小鼠肝组织甘油三酯浓度、中性粒细胞、iNOS 蛋白浓度和早期胰岛素抵抗迹象显著减弱，而 FFC + B 喂养的小鼠则明显减弱（所有 P 值均<0.05）。这些发现与 Adipor1 mRNA 表达的超诱导（与所有其他组相比增加了+ ~ 18 倍）以及 FFC + B 喂养小鼠肝组织脂质过氧化标志物的减少有关，而与 FFC 喂养的动物相比。FFC 和 FFC + E 喂养的小鼠之间未发现类似的差异。用啤酒（相当于 2 mmol/L 乙醇）处理的 J774A.1 细胞中，Adipor1 的表达也被超诱导（7.5 倍）。
这些数据表明，适量饮用发酵酒精饮料（如啤酒）至少部分通过与肝 AdipoR1 表达相关的机制减轻 NAFLD 的发展。
