Public Release: 

Tribble 3 can induce nonalcoholic fatty liver disease?

World Journal of Gastroenterology

Three pseudo kinases of the Tribbles family have been recently recognized, which include TRB1, TRB2 and TRB3. Recent research has found that the expression of hepatic TRB3 increased in a rat model of diabetes. TRB3 could block the insulin signaling pathway through inhibiting Akt activation, which contributes to insulin resistance.

A research article to be published on May 21, 2009 in the World Journal of Gastroenterology addresses this question. This research, lead by Dr. Yu-Gang Wang and his colleagues in the Department of Gastroenterology, Shanghai Changning Central Hospital, China, used real-time fluorescent quantitative reverse transcription-polymerase chain reaction technology and Western blotting analysis to study the protein expression of TRB3mRNA, Akt and phosphorylation protein kinase B during the progression of NAFLD.

The expression level of TRB3mRNA in NAFLD rats was significantly higher than in normal controls. Also, the expression levels of Akt and p-Akt-Thr308 in NAFLD rats was significantly lower than the control group. Since TRB3 can block insulin signaling pathway through inhibiting Akt activation, which contributes to insulin resistance, it may be an important factor in the occurrence and development of NAFLD. This study provides an experimental basis for future studies on the role of TRB3 in NAFLD. The control of the expression level of TRB3 in liver may become a new target for NAFLD therapy.


Reference: Wang YG, Shi M, Wang T, Shi T, Wei J, Wang N, Chen XM. Signal transduction mechanism of TRB3 in rats with non-alcoholic fatty liver disease. World J Gastroenterol 2009; 15(19): 2329-2335

Correspondence to: Dr. Xi-Mei Chen, Department of Gastroenterology, Tongji Hospital of Tongji University, Shanghai 200065, China.

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 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.

About The WJG Press

The WJG Press mainly publishes World Journal of Gastroenterology.

Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.