1 The present results support the link between BT and systemic circulatory dysfunction check details in cirrhosis, suggesting that intestinal decontamination could enhance the hemodynamic effects of terlipressin and contribute to a decrease in rebleeding events in patients with variceal bleeding taking antibiotic prophylaxis.7 Georgios N. Kalambokis M.D.*, Athanasia Mouzaki M.D., Ph.D.‡, Maria Rodi M.D.‡, Konstantinos Pappas M.D.†, Epameinondas V. Tsianos M.D., Ph.D.*, * First Division of Internal Medicine and Hepato-Gastroenterology Unit, Ioannina, Greece, † Department of Cardiology, Medical School of Ioannina, Ioannina, Greece, ‡ Division of Hematology, Department of

Internal Medicine, Medical School, University of Patras, Patras, Greece. “
“We read with great interest the article entitled “Toll-like receptor 4 is involved in the development

of fructose-induced hepatic steatosis in mice”, published in a recent issue of HEPATOLOGY.1 In this study, Spruss et al. verified the hypothesis that Toll-like receptor 4 (TLR-4) may play a central role in the onset of fructose-induced nonalcoholic fatty liver disease (NAFLD). To this aim, the authors used wild-type (C3H/HouJ) mice and TLR-4 mutant (C3H/HeJ) mice, both fed plain water or 30% fructose-enriched solution for 8 weeks. As already described by other studies,2, 3 chronic intake of 30% fructose solution leads to hepatic steatosis and some features of metabolic syndrome in wild-type animals, including the increase of body and liver weight, hepatic triglyceride levels, and this website plasma levels of alanine aminotransferase (ALT). Interestingly, TLR-4 mutants fed water presented only a weak decrease of Astemizole liver weight and hepatic triglycerides with respect to wild-type animals fed water, and the enrichment with fructose exclusively caused the restoration of the significantly increased levels of these two parameters. These results clearly suggest that the presence of TLR-4 is essential to explain liver damage, body weight gain, and ALT impairment due to the fructose intake. Furthermore, the

authors found that plasma endotoxin levels were significantly increased both in wild-type and mutant mice fed chronically with a 30% fructose solution, in comparison to water-fed controls. The role of fructose in NAFLD development was not entirely unknown to researchers. In particular, a recent work4 demonstrates that patients with NAFLD have a significantly greater consumption of fructose than controls, and an increased hepatic expression of fructokinase messenger RNA. Although the role of TLR-4 in carbohydrate-dependent NAFLD has been only recently suggested by Thuy and colleagues,5 they have pinpointed one of the potential mechanisms through which fructose could participate in NAFLD development and progression in humans: a carbohydrate-rich diet may produce ethanol when intestinal stasis favors bacterial overgrowth in the upper parts of the gastrointestinal tract.