Probiotics and antibodies to TNF inhibit inflammatory activity and improve nonalcoholic fatty liver disease
By Zhiping Li, Shiqi Yang, Huizhi Lin, Jiawen Huang, P. Watkins, A. Moser, C. Desimone, Xiao-yu Song, A. Diehl. Hepatology, 2003
948 citations recorded by the source corpus.
Subfields: Endocrinology, Diabetes and Metabolism, Epidemiology, Pathology and Forensic Medicine
View Paper: https://www.semanticscholar.org/paper/bb8982a62b8b79a0bb844cb88841c65c7fee0929
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In Endocrinology, Diabetes and Metabolism
In Epidemiology
In Pathology and Forensic Medicine
Citations in the corpus
- Toll-like receptor-4 signaling and Kupffer cells play pivotal roles in the pathogenesis of non-alcoholic steatohepatitis. (2007, background): “Attenuation of CCl(4)induced hepatic fibrosis by GdCl(3) treatment or dietary glycine.”
- Systemic inflammation in nonalcoholic fatty liver disease is characterized by elevated levels of CCL2. (2006, background): “Thus, while several studies have explored the role of TNF-a in these disorders [7,10,11], much less focus has been directed against the possible involvement of other inflammatory mediators.”
- Increased intestinal permeability and tight junction alterations in nonalcoholic fatty liver disease (2009, neutral): “n 17 18 14 21 Sex (M) 3/14 2/16 NS 3/11 2/19 NS Age 44 (34-53) 41 (32-54) NS 46(32-54) 40 (32-53 NS BMI 24.”
- Evolution of inflammation in nonalcoholic fatty liver disease: The multiple parallel hits hypothesis (2010, background): “Anti-TNF antibody treatment and metformin, an antidiabetic drug that inhibits hepatic TNFa expression, improve steatosis in ob/ob mice.(23,24) Other proinflammatory mediators might also contribute to the development of steatosis because in some studies hepatic steatosis was not dependent on TNFa.”