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LETTER |
1 Department of Histology, Microbiology, and Medical Biotechnologies, and Department of Gastroenterological Sciences, University of Padua, Italy
2 Department of Histology, Microbiology, and Medical Biotechnologies, University of Padua, Italy
3 Department of Gastroenterological Sciences, University of Padua, Italy
4 Department of Histology, Microbiology, and Medical Biotechnologies, University of Padua, Italy
5 Department of Gastroenterological Sciences, University of Padua, Italy
Correspondence to:
Correspondence to:
Dr I Castagliuolo
University of Padua, School of Pharmacy, Department of Histology, Microbiology, and Medical Biotechnology, Via A Gabelli 63. Padua, 35121 Italy; ignazio.castagliuolo@unipd.it
Keywords: Non-alcoholic steatohepatitis; endotoxin; obesity; polymorphism; CD14
| The first 150 words of the full text of this article appear below. |
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 portal blood (P Brun, manuscript submitted). Circulating LPS binds to soluble and cell membrane receptors, such as CD14 and toll-like receptor 4 (TLR4), leading to release of inflammatory
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P. Brun, I. Castagliuolo, V. D. Leo, A. Buda, M. Pinzani, G. Palu, and D. Martines Increased intestinal permeability in obese mice: new evidence in the pathogenesis of nonalcoholic steatohepatitis Am J Physiol Gastrointest Liver Physiol, February 1, 2007; 292(2): G518 - G525. [Abstract] [Full Text] [PDF] |
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