Kanuri Giridhar, Wagnerberger Sabine, Landmann Marianne, Prigl Eva, Hellerbrand Claus, Bischoff Stephan C, Bergheim Ina
Department of Nutritional Sciences, Model Systems of Molecular Nutrition, Friedrich-Schiller-University Jena, Dornburger Str. 25, 07743, Jena, Germany.
Eur J Nutr. 2015 Apr;54(3):465-74. doi: 10.1007/s00394-014-0730-z. Epub 2014 Jun 15.
The aim of the present study was to assess whether the effects of acute consumption of stout or pilsner beer on the liver differ from those of plain ethanol in a mouse model.
Seven-week-old female C57BL/6J mice received either ethanol, stout or pilsner beer (ethanol content: 6 g/kg body weight) or isocaloric maltodextrin solution. Plasma alanine transaminase, markers of steatosis, lipogenesis, activation of the toll-like receptor-4 signaling cascade as well as lipid peroxidation and fibrogenesis in the liver were measured 12 h after acute ethanol or beer intake.
Acute alcohol ingestion caused a marked ~11-fold increase in hepatic triglyceride accumulation in comparison to controls, whereas in mice exposed to stout and pilsner beer, hepatic triglyceride levels were increased only by ~6.5- and ~4-fold, respectively. mRNA expression of sterol regulatory element-binding protein 1c and fatty acid synthase in the liver did not differ between alcohol and beer groups. In contrast, expression of myeloid differentiation primary response gene 88, inducible nitric oxide synthases, but also the concentrations of 4-hydroxynonenal protein adducts, nuclear factor κB and plasminogen activator inhibitor-1 were induced in livers of ethanol treated mice but not in those exposed to the two beers.
Taken together, our results suggest that acute ingestion of beer and herein especially of pilsner beer is less harmful to the liver than the ingestion of plain ethanol.
本研究旨在评估在小鼠模型中,急性饮用烈性黑啤酒或比尔森啤酒对肝脏的影响是否与单纯摄入乙醇不同。
7周龄雌性C57BL/6J小鼠分别接受乙醇、烈性黑啤酒或比尔森啤酒(乙醇含量:6克/千克体重)或等热量的麦芽糊精溶液。在急性摄入乙醇或啤酒12小时后,检测血浆丙氨酸转氨酶、肝脂肪变性标志物、脂肪生成、Toll样受体4信号级联激活以及肝脏中的脂质过氧化和纤维化情况。
与对照组相比,急性摄入酒精导致肝脏甘油三酯积累显著增加约11倍,而在饮用烈性黑啤酒和比尔森啤酒的小鼠中,肝脏甘油三酯水平仅分别增加约6.5倍和4倍。酒精组和啤酒组肝脏中固醇调节元件结合蛋白1c和脂肪酸合酶的mRNA表达没有差异。相反,乙醇处理小鼠的肝脏中诱导了髓样分化初级反应基因88、诱导型一氧化氮合酶的表达,同时4-羟基壬烯醛蛋白加合物、核因子κB和纤溶酶原激活物抑制剂-1的浓度也升高,而饮用两种啤酒的小鼠肝脏中未出现这种情况。
综上所述,我们的结果表明,急性饮用啤酒,尤其是比尔森啤酒,对肝脏的危害小于单纯摄入乙醇。