Nature Communication published a recent research on hepatic metabolism by the research group led by Professor Li Hongliang, from Animal Experiment Center of Wuhan University.
The paper is entitled “Hepatocyte TRAF3 Promotes Liver Steatosis and Systemic Insulin Resistance Through Targeting TAKI-dependent Signalling”, with doctoral student Wang Pixiao and Professor Li Hongliang as the first author and the corresponding author respectively. This research finding is funded by National Science Foundation for Distinguished Young Scholars, National Science & Technology Support Plan and National Natural Science Foundation of China.
The research finds that TRAF3 also plays a critical role on liver steatosis and insulin resistance.
Nonalcoholic fatty liver disease (NAFLD) is among the common chronic liver diseases, which can gradually develop into nonalcoholic steatohepatitis(NASH) and result in cirrhosis and hepatic carcinoma. TRAF3 is a member of tumor necrosis factor receptor-associated factor family. Previous researches focused on functions of TRAF3 on innate immune activation and regulation of inflammatory cell and inflammatory response. However, its function in hepatocyte and its mechanism and regulation to NAFLD relating to chronic inflammation still remain uncertain.
This research reveals that TRAF3 can promote fatty degeneration of liver and aggravate hepatic metabolic disorder due to its influence on chronic inflammation induced by high fat diet, insulin resistance and dysglycemia. The research also shows that reducing the expression of hepatocyte TRAF3 or damaging its signaling pathways may become an effective disease prevention strategy for NAFLD and other related metabolic disorders. This study is of great significance as it offers a deeper understanding of hepatic metabolic disorder, providing a new way of thinking and important theoretical basis for the prevention and treatment of the diseases in question.
(Rewritten by Yuxuan Zhu, Edited by Jiahao Xiang & Sijia Hu)
