Research Interests

• Epidemiological studies indicate that patients with diabetes mellitus have an increased risk of non-alcoholic steatohepatitis(NASH). Diabetic patients have increased level of advanced glycation end products(AGEs) which might play a rolein liver injury and NASH. However, the underlying mechanism remains unclear. Our preliminary work showed that AGEs induced hepatocyte injury. Western blot analysis indicated that the expression of ChREBP, a glucose responsive transcription factor regulating cell metabolism and proliferation, is increased in AGE-treated hepatocytes. Deletion of ChREBP also reduced DEN induced liver cell DNA damage. Based on our study, we aim to find out the molecular mechanism by which AGEs induce ChREBP expression and the role of ChREBP in liver injury induced by AGEs.