Therefore, the present study aimed to evaluate the effect of BBR on abnormal GMC proliferation in DN and to further explore the underlying mechanism and relationship among BBR, abnormal GMC proliferation, the PI3K/Akt pathway and GLUT1 alterations, which will offer insights into controlling cellular responses to hyperglycaemia that initiate the progression of DN. The gene discussed is SLC2A1; the disease is liver dysplastic nodule.