Brief Article
Copyright ©2011 Baishideng Publishing Group Co.
World J Gastroenterol. Oct 21, 2011; 17(39): 4434-4439
Published online Oct 21, 2011. doi: 10.3748/wjg.v17.i39.4434
Figure 1
Figure 1 Expression of glucose transporter type 2 and apical glucose transporter type 2 in the small intestinal mucosa. A: In normal control rats, glucose transporter type 2 (GLUT2) mainly resides at the BLM (arrows); B: In obese rats, the GLUT2 and apical GLUT2 expression was increased (arrows) compared to the controls; C: In octreotide-treated rats, GLUT2 and apical GLUT2 expression was significantly decreased (arrows) compared to non-treated obese rats. Magnification: × 400.
Figure 2
Figure 2 Expression of glucose transporter type 2 mRNA in the small intestinal mucosa. Obese rats showed increased mRNA levels of glucose transporter type 2 (GLUT2) when compared with the controls, whereas octreotide-treated rats showed decreased levels of GLUT2 mRNA, when compared with obese rats. Total RNA was analyzed by reverse transcriptase polymerase chain reaction. House-keeping gene GAPDH was used as an internal control.
Figure 3
Figure 3 Expression of glucose transporter type 2 protein by Western blotting. Obese rats showed increased protein levels of glucose transporter type 2 (GLUT2) when compared with the controls, whereas the octreotide-treated rats showed decreased levels of GLUT2 protein, when compared with obese rats. β-actin was used as an internal loading control.