GLUT2 Antibody - #DF7510

Fig. 7. LBT treatment activated the PI3K/Akt pathway in the liver of hyperglycemic and insulin-resistant mice and insulin-resistant HepG2 cells. (A) Hepatic immunohistochemical analysis of PI3K p85, pAkt and Akt protein expressions, (B) Cellular western blotting analysis of GLUT2, PI3K p85 and Akt protein expressions. Different letters represent a significant difference among multiple groups, * represents a significance compared with the Control group, # represents a significance between two groups, ns represents no significance. #,*, p < 0.05; ##, **, p < 0.01.

Figure 5 RH reduced brain GLUT3-mediated glucose uptake in STZ-induced APP/PS1-DM mice. (A) Representative PET/CT images showing in vivo brain 18F-FDG uptake (coronal, sagittal, and transaxial sections, n = 6 mice for each group). Cor, Cortex; Hip, hippocampus; Mid, midbrain; HPOA, hypothalamus; BS, brain stem; Cer, cerebellum; OB, Olfactory Bulb; BF, basal forebrain; Tha, thalamus; SC, superior colliculi; CG, central gray; Str, striatum. (B) Quantification for SUV of 18F-FDG in brain region (n = 6 for mice for each group). (C) Western blot and quantitation for GLUT1, GLUT2, GLUT3, GLUT4, GLUT5, SGLT1, and SGLT2 in hippocampal homogenates (n = 3 mice for each group). The data are expressed as the mean ± SEM. Statistical significance was assessed using unpaired Student’s t test. *P < 0.05 and **P < 0.01, APP/PS1-DM versus APP/PS1; #P < 0.05 and ##P < 0.01, APP/PS1-DM-RH versus APP/PS1-DM; WT versus APP/PS1; NS, no significant difference.

Fig. 3. |Cell dysfunction caused by GP is improved in MKP-5 overexpressing MIN6 cells. (B, C) MIN6-PC and MIN6-MKP5 cells were stimulated with GP for 24 h. The phosphorylation of AKT and the expression of GLUT-2 were assessed by western blotting (B). Relative levels of PDX-1 and GCK mRNA were quantified by real-time PCR analysis (C). Data are given as means ± SEM. *, P < 0.05.

Fig. 3 Receptor–ligand interactions of compound. a Protocol flowchart of MYC inhibitor discovery strategy, ten candidate inhibitors including okanin were screened at last through HTV, SP,and XP screen methods. b Binding model of MYC–DNA complexes with okanin (PDB code: 1NKP) through molecular docking method.The results showed that okanin interacted with two key amino acid residues in the DNA binding site of MYC. c Okanin could significantly inhibit the transcriptional regulatory activity of MYC by luciferase assay. d Okanin significantly inhibited the expressions of GLUT2 and p65, which were the downstream proteins of MYC(n = 3, **P \0.01)

Figure 11 Effect of YQ on insulin secretion-related proteins in pancreas islet. The expressions levels of IRS-2, P-PI3K, PI3K, P-Akt, Akt, and GLUT4 were assessed by western blot analysis. The results are shown as means ± SEM (n = 9–10). ##P < 0.01 compared with the control group; ∗P < 0.05, ∗∗P < 0.01 compared with the model group.