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Non-alcoholic fatty liver (NAFL) is a common hepatic disorder that progresses to non-alcoholic steatohepatitis (NASH) in only 20% of patients. Whereas polymorphisms in genes involved in fat metabolism confer susceptibility to NAFL,1 the risk factors involved in the progression of the disease to NASH are not known. A possible role for intestinal derived bacterial endotoxins in the progression from NAFL to NASH is gaining increasing interest in view of recent experimental data. Thus NASH patients show a higher prevalence of small intestinal bacterial overgrowth (SIBO) and, in animal models of SIBO, hepatitis is improved following antibiotic treatment.2,3 Furthermore, we have recently observed that increased intestinal mucosal permeability, such as that observed in obese C57BL/6Job/ob mice, leads to higher lipopolysaccharide (LPS) levels in …
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