The role of small intestinal bacterial overgrowth, intestinal permeability, endotoxaemia, and tumour necrosis factor α in the pathogenesis of non-alcoholic steatohepatitis

By A. Wigg, I. Roberts-Thomson, R. Dymock, P. McCarthy, R. Grose, A. Cummins. Gut, 2001

862 citations recorded by the source corpus.

Subfields: Epidemiology, Molecular Biology, Pathology and Forensic Medicine

View Paper: https://www.semanticscholar.org/paper/f9a3ea0fabaa2a1b4d0d2621820d22f8c5c5795e

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. P. Newsome
2. J. Tomlinson
3. J. Dowman
4. M. Pinzani
5. E. Tsochatzis
6. E. Buzzetti
7. Patrice D Cani

In Molecular Biology

1. Cesare Furlanello
2. Paola Paci
3. Patrice D Cani

In Pathology and Forensic Medicine

1. M. Pinzani

Citations in the corpus

• Increased intestinal permeability in obese mice: new evidence in the pathogenesis of nonalcoholic steatohepatitis. (2007, background): “Although it is an intriguing hypothesis, the potential role of intestinal endotoxins in liver damage is based only on indirect evidence (47, 55).”
• Pathogenesis of non-alcoholic fatty liver disease (2009, background): “Small intestinal bacterial overgrowth and increased gut permeability have been found more frequently in patients with NASH when compared with controls.(81,82) This has led to the suggestion that this may explain the onset of NASH and liver fibrosis as a complication of jejunoileal bypass surgery.”
• Toll-like receptor-4 signaling and Kupffer cells play pivotal roles in the pathogenesis of non-alcoholic steatohepatitis. (2007, background): “Gastroenterology 1979 Apr;76(4):710–719.”
• Gut microbiota profiling of pediatric nonalcoholic fatty liver disease and obese patients unveiled by an integrated meta‐omics‐based approach (2017, background): “Thus, quantitative and qualitative variations in the bacteria that compose the gut microbiota may actively contribute to the pathogenesis of several liver diseases, including nonalcoholic fatty liver disease (NAFLD), alcoholic steatohepatitis, and cirrhosis.((2-7)) NAFLD is one of the most common ca”
• The multiple-hit pathogenesis of non-alcoholic fatty liver disease (NAFLD). (2016, background): “The significant correlation between intestine bacterial overgrowth and NASH is observed even in the absence of increased mucosal permeability [139].”
• Role of Kupffer cells in host defense and liver disease (2006, result): “In line with these observations a recent study reported a high frequency of small intestinal bacterial over- growth in patients with NASH (123) suggesting that gut-derived portal endotoxin may be an important stimulus for KC activation in NAFLD.”
• Increased intestinal permeability and tight junction alterations in nonalcoholic fatty liver disease (2009, neutral): “9) 0 Villi ZO-1 nuclei (%) 7 (4-12) 1 (0-3) 0.”