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10th Euro-Global Conference on Infectious Diseases

Rome, Italy

Huseyin Kayadibi

Huseyin Kayadibi

Hitit University, Turkey

Title: The role of intestinal microbiota in the pathogenesis of non-alcoholic Steatohepatitis

Biography

Biography: Huseyin Kayadibi

Abstract

Non-alcoholic steatohepatitis (NASH) is determined as the fatty liver with inflammation and fibrosis that resembles the alcoholic liver disease without the history of alcohol ingestion. Genetic and environmental factors are important in the pathogenesis of NASH. However, it is still unclear why some thin individuals develop NASH, while some obese individuals do not. Intestinal microbiota may be important in these situations. Because, microorganisms have some effects on energy homeostasis, activation of pro-inflammatory mediators and metabolism of bile acids, short chain fatty acids, choline and alcohol. Intestinal barrier components, tight junction, zonula adherence, desmosome, gap junction, integrin, selectin and cell adhesion molecule have very important roles in the gut liver axis for healthy liver. Because of intestinal barrier dysfunction causes the increased transfer of toxic metabolites to the liver from gut by the gut-liver axis. Increased levels of these substances in liver induce the multiple inflammatory processes by the activation of toll like receptors and nod like receptors that may result with the hepatitis and fibrosis. Microbial imbalance called dysbiosis may cause to the development of leaky gut and then NASH. In previously published articles, it was shown that intestinal dysbiosis and NASH are related with the lower prevalence of Bacteroidetes and higher prevalence of Firmicutes. Therefore, the species of microbiota may be important for elucidation of the pathogenesis of NASH. It was also shown that diversity of the intestinal microbiota has a key role for the pathogenesis of liver diseases. In future, studies with liver biopsy proven NASH patients will elucidate the role of intestinal microbiota and related metabolic components in the pathogenesis of NASH.