maltodextrin and Fatty-Liver

In experimental animals, recent results suggest that the addition of inulin-type fructans such as oligofructose (OFS) in the diet decreases triacylglycerol accumulation in the liver tissue. Therefore, we have investigated the effect of daily ingestion of OFS in seven patients with nonalcoholic steatohepatitis (NASH), confirmed by liver biopsies.. They received 16 g/day OFS or maltodextrine (placebo) for 8 weeks in a randomized double-blind crossover design. Energy intake, body composition, liver steatosis and blood parameters were analysed after 4 and 8 weeks of dietary supplementation.. Compared to placebo, OFS decreased significantly serum aminotransferases, aspartate aminotransferase after 8 weeks, and insulin level after 4 weeks, but this could not be related to significant effect on plasma lipids.. This pilot study supports the putative interest of OFS in the management of liver diseases associated with abnormal lipid accumulation in humans.

Topics: Adult; Aged; Aspartate Aminotransferases; Biopsy; Body Composition; Cross-Over Studies; Double-Blind Method; Energy Intake; Fatty Liver; Glucose; Hepatitis; Humans; Insulin; Lipid Metabolism; Liver; Male; Middle Aged; Oligosaccharides; Pilot Projects; Polysaccharides; Time Factors; Transaminases

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