XXXX , @entity409 and intestinal microbiota.

@entity32 @entity82 @entity1560 @entity28 @entity409 @entity1877 @entity1561 @entity6741 @entity209 @entity157 @entity375 @entity1068
@entity1561 ( @entity1561 ) is a chronic @entity409 that is increasing in prevalence with the worldwide epidemic of @entity28 . @entity1561 is the hepatic manifestation of the @entity209 . The term @entity1561 describes a spectrum of liver pathology ranges from simple @entity1560 to @entity1560 with @entity32 and even @entity82 . @entity209 and @entity1561 also predict @entity157 . Many genetic and environmental factors have been suggested to contribute to the development of @entity28 and @entity1561 , but the exact mechanisms are not known. Intestinal ecosystem contains trillions of microorganisms including bacteria, Archaea, @entity375 and viruses. Several studies support the relationship between the intestinal microbial changes and @entity28 and also its complications, including insulin resistance and @entity1561 . Given that the gut and liver are connected by the portal venous system, it makes the liver more vulnerable to translocation of bacteria, bacterial products, endotoxins or secreted cytokines. Altered intestinal microbiota (dysbiosis) may stimulate hepatic fat deposition through several mechanisms: regulation of gut permeability, increasing low-grade @entity32 , modulation of dietary @entity1877 metabolism, regulation of @entity6741 metabolism and producing endogenous @entity1068 . Regulation of intestinal microbial ecosystem by diet modifications or by using probiotics and prebiotics as a treatment for @entity28 and its complications might be the issue of further investigations.
