FA inhibited the expression of GLUT2 in diabetic rats by affecting the interactions between the GLUT2 gene promoter and the transcription factors involving the sterol regulatory element-binding protein-1c (SREBP-1c), the hepatocyte nuclear factors (HNF) 1α and HNF 3β, and then produced therapeutic effects on diabetes [63] (Figure 2). This evidence concerns the gene SLC2A2 and diabetes mellitus.