How did glycine significantly decrease liver injury?

October 31, 2008

The nonessential amino acid glycine has been shown to be anti-inflammatory in several animal injury models. Recent studies demonstrated that dietary glycine protected both the lung and liver against lethal doses of endotoxin in rat or other animals and improved graft survival after liver transplantation. The influence of dietary glycine on oxidant-induced or cholestatic liver injury was not known.

A research article to be published on October 21, 2008 in the World Journal of Gastroenterology addresses this question. The research team led by Prof. Thurman from the University of North Carolina used a dietary and cholestatic model thru BDL in rats to address this question. They could demonstrate that hepatic injury due to BDL is significantly reduced by dietary glycine in rats. Moreover, the data indicated that glycine decreases liver injury under the conditions of experimental cholestasis thru a direct effect on hepatocytes. Surprisingly, Kupffer cells did not appear to play a major role in the pathological changes caused by cholestasis.

It is best known that Kupffer cells, the resident macrophages of the liver, are involved in several disease states, such as endotoxin shock, alcoholic liver diseases, and other toxicant-induced liver injury by releasing eicosanoids, inflammatory cytokines, and free radical species. Furthermore, in previous studies of the research team, a glycine-dependent chloride channel on the cell membrane of Kupffer cells and other macrophages that influence the activation process of these cells could be detected. But in the actual used cholestatic model no significant influence of this cell line on liver injury could be detected.
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Reference: Froh M, Zhong Z, Walbrun P, Lehnert M, Netter S, Wiest R, Conzelmann L, Gäbele E, Hellerbrand C, Schölmerich J, Thurman RG. Dietary glycine blunts liver injury after bile duct ligation in rats. World J Gastroenterol 2008; 14(39): 5996-6003

http://www.wjgnet.com/1007-9327/14/5996.asp

Correspondence to: Matthias Froh, Department of Internal Medicine I, University of Regensburg, Regensburg 93042, Germany. froh.science@mac.com Telephone: +49-941-9447012 Fax: +49-941-9447011

About World Journal of Gastroenterology

World Journal of Gastroenterology (WJG), a leading international journal in gastroenterology and hepatology, has established a reputation for publishing first class research on esophageal cancer, gastric cancer, liver cancer, viral hepatitis, colorectal cancer, and H pylori infection. It provides a forum for both clinicians and scientists. WJG has been indexed and abstracted in Current Contents/Clinical Medicine, Science Citation Index Expanded (also known as SciSearch) and Journal Citation Reports/Science Edition, Index Medicus, MEDLINE and PubMed, Chemical Abstracts, EMBASE/Excerpta Medica, Abstracts Journals, Nature Clinical Practice Gastroenterology and Hepatology, CAB Abstracts and Global Health. ISI JCR 2003-2000 IF: 3.318, 2.532, 1.445 and 0.993. WJG is a weekly journal published by WJG Press. The publication dates are the 7th, 14th, 21st, and 28th of every month. The WJG is supported by The National Natural Science Foundation of China, No. 30224801 and No. 30424812, and was founded with the title China National Journal of New Gastroenterology on October 1, 1995, and renamed WJG on January 25, 1998.

About The WJG Press

The WJG Press mainly publishes World Journal of Gastroenterology.

World Journal of Gastroenterology

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