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.
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