Is the intestinal mucosa barrier malfunction involved in nonalcoholic steatohepatitis?

The pathogenesis of NASH remains unclear. Nowadays, lipid metabolism abnormality, insulin resistance and oxidative stress and lipid peroxidation reaction are thought to place an important role in the pathogenesis of NASH. Several researches have also demonstrated that the change of intestinal environment may play a role in NASH, which may be a cause of enterogenous endotoxemia. While the relationship between intestinal mucosa barrier function and NASH is uncertain.

A research article to be published on 28 May 2008 in the World Journal of Gastroenterology addresses this question. The research team led by Wan-Chun Wu from Yijishan Hospital established an NASH animal model by fat-rich diet to explore the change of intestinal mucosa barrier function in the progress of NASH.

Several researches have demonstrated that the change of intestinal environment may play a role in NASH, which may be a cause of enterogenous endotoxemia. While the relationship between intestinal mucosa barrier function and NASH is uncertain. This article describes an animal experiment of NASH.

Dr. Wan-Chun Wu et al established NASH animal model by high-fat diet for 12 week successfully. The level of endotoxin, D-xylose, TG, TC, ALT and AST, intestinal tissue SOD and MDA as well as intestinal mucus sIgA were measured. Liver pathologic score was calculated to qualify the severity of hepatitis. Serum ALT, AST levels were detected to evaluate the severity of hepatitis.

At the end of 8th week, there are no marked changes the level of endotoxin, D-xylose and sIgA of model group than those of control group. At the end of 12th wk, the rats presented the pathology of steatohepatitis with higher serum levels of endotoxin, D-xylose in model group than those of control group. The intestinal mucosal fluid level of sIgA of model group decreased markedly than those of the end of 12th week control group. And Portal vein serum endotoxin level has a positive correlation with abdominal aorta serum D-xylose level and a negative correlation with intestine mucus sIgA level. Rats in model group with higher MDA contents and lower SOD activity in intestinal tissue than rats in control group at 8,12th week. The results suggest that it may exist the intestinal mucosa barrier destruction, which may one of important factors in the the pathogenesis and progress of NASH. And the pathogenesis of intestinal mucosa barrier damage is possible induced by intestinal tissue lipid peroxidation reaction increasing.

The results of this study suggest a promising future for many NASH patients. The results demonstrate a new view of the pathogenesis of NASH and have significance for treatment.

Reference: Li S, Wu WC, He CY, Han Z, Jin DY, Wang L. Change of intestinal mucosa barrier function in the progress of non-alcoholic steatohepatitis in rat World J Gastroenterol 2008;14(20): 3254-3258:
http://www.wjgnet.com/1007-9327/14/3254.asp

Correspondence to: Wan-Chun Wu, Department of Gastroenterology, Yijishan Hospital, Wuhu 241001, Anhui Province, China. wwch5182000@yahoo.com.cn
Telephone: +86-553-5739106 Fax: +86-553-5738401

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 and 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 day of every month. WJG is supported by The National Natural Science Foundation of China, No. 30224801 and No. 30424812, and was founded with the name of China National Journal of New Gastroenterology on October 1, 1995, and renamed WJG on January 25, 1998.