Transforming growth factor beta-1 upregulates glucose transporter 1 and glycolysis through canonical and noncanonical pathways in hepatic stellate cells

Figure 1 Glucose transporter 1 expression is correlated with liver fibrosis progression. A-D: The classic mouse model of CCl₄-induced liver fibrosis was used to first clarify whether glucose transporter 1 (GLUT1) is related to liver fibrosis. Sirius red staining and alpha-smooth muscle actin (α-SMA) immunohistochemical (IHC) staining were used to confirm that the liver fibrosis model was successfully established, and then the mice were randomly divided into the CCl₄ group and the control oil group (n = 6-10 mice/group) (A); Evaluation of liver fibrosis using Sirius red staining (B); Determination of the area ratio of positive IHC staining for α-SMA in the mouse CCl₄-induced liver fibrosis model (C); GLUT1 expression was more abundant in the liver tissue samples from the model group (D); E and F: Immunofluorescence staining for GLUT1 (red) and α-SMA (green) in the CCl₄ model. Cell nuclei were counterstained with DAPI. Scale bar for immunofluorescence staining, 200 μm; scale bars for IHC staining and Sirius red staining, 200 μm; G: IHC staining for α-SMA and GLUT1 in the healthy control and liver fibrosis groups (scale bar, 100 μm); H: Western blot analysis of changes in GLUT1 protein levels in the oil group and the CCl₄ model group; I: Western blot analysis of GLUT1 protein expression in human liver tissues from the healthy control group and the liver fibrosis group. Data in B-D, G and H are presented as the mean ± SE. Statistically significant differences were detected (compared with the oil group, ^aP < 0.05 and ^bP < 0.01; compared with the healthy control group, ^dP < 0.05). GLUT1: Glucose transporter 1; α-SMA: Alpha-smooth muscle actin.