4-hydroxy-2-nonenal and maltodextrin

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.

Topics: Alanine Transaminase; Aldehydes; Animals; Beer; Biomarkers; Disease Models, Animal; Ethanol; Fatty Liver; Female; Lipid Peroxidation; Lipogenesis; Liver; Mice; Mice, Inbred C57BL; Myeloid Differentiation Factor 88; NF-kappa B; Nitric Oxide Synthase Type II; Plasminogen Activator Inhibitor 1; Polysaccharides; RAW 264.7 Cells; RNA, Messenger; Sterol Regulatory Element Binding Protein 1; Toll-Like Receptor 4; Triglycerides