INT55291
From wiki-pain
|
|
|
|
|
Sentences Mentioned In
Key: | Protein | Mutation | Event | Anatomy | Negation | Speculation | Pain term | Disease term |
Strikingly, however, overexpression of GLUT-1 in muscle induced a profound reduction in insulin-stimulated whole body glucose disposal. | |||||||||||||||
| |||||||||||||||
|
Fasted mice overexpressing GLUT-1 in skeletal muscle exhibited a GIR that was only 54% that of controls (19.3 +/- 1.8 vs. 36.0 +/- 3.9 mg.kg-1.min-1) when blood glucose was clamped at euglycemic values. | |||||||||||||||
| |||||||||||||||
|
The effect of glucose transporter expression on insulin-stimulated whole body glucose disposal was examined in transgenic mice overexpressing GLUT-1 or GLUT-4. | |||||||||||||||
| |||||||||||||||
|
Differential effects of GLUT-1 or GLUT-4 overexpression on insulin responsiveness in transgenic mice. | |||||||||||||||
| |||||||||||||||
|
This downregulation of Glut-1 expression in the endothelial cells of the BSCB may be related to altered endothelial lining leading to vascular leakage. | |||||||||||||||
| |||||||||||||||
|
Downregulation of Glut-1 and CD146 expressions in spinal cord endothelial cells was also found in G93A mice at early and late stage disease and may relate to altered endothelial lining leading to vascular leakage. | |||||||||||||||
| |||||||||||||||
|
In the present study, we found low and mostly absent expression of Glut-1 in capillaries of both cervical and lumbar spinal cords of G93A mice at early and late stages of disease. | |||||||||||||||
| |||||||||||||||
|
Although additional experiments such as quantitative analysis of Glut-1 distribution and density in the endothelial plasma membranes are needed to elucidate the regulatory mechanisms of Glut-1 expression in the spinal cord, the present study indicates that alteration of Glut-1 could be involved in the pathogenesis of ALS. | |||||||||||||||
| |||||||||||||||
|
Alternatively, decreased Glut-1 expression may result from aggravated alterations of the BSCB in G93A mice. | |||||||||||||||
| |||||||||||||||
|
Glut-1 expression was increased in WT and eNOS KO mice. | |||||||||||||||
| |||||||||||||||
|
Additionally, downregulation of Glut-1 and CD146 expressions in the endothelial cells of the BSCB may be related to altered endothelial lining leading to vascular leakage. | |||||||||||||||
| |||||||||||||||
|
Additionally, downregulation of Glut-1 and CD146 expressions in the endothelial cells of the BSCB were found which may relate to vascular leakage.
| |||||||||||||||
| |||||||||||||||
|
In search for the signs of BBB damage in the brain of symptomatic A53T mice, we examined the expression and subcellular distribution of aquaporin 4, glucose transporter 1 (Glut1) and von Willebrand factor (vWF) in astrocyte and vascular endothelial cells. | |||||||||||||||
| |||||||||||||||
|
50, Chemicon), rabbit anti-mouse Glut-1 polyclonal antibody (1? | |||||||||||||||
| |||||||||||||||
|
Immunofluorescent staining for Glut-1 (glucose transporter 1) showed high expression of Glut-1 in microvascular endothelia of the cervical and lumbar ventral horn of the spinal cords in C57BL/6J mice at 1213 weeks of age (Figure 8A, B, H, I) and at 1920 weeks of age (Figure 8C, J). | |||||||||||||||
| |||||||||||||||
|
The expression of GLUT4 or GLUT1 was not modified by chronic treatment with IL-6 (Fig. 2E). | |||||||||||||||
| |||||||||||||||
|
Cells were submitted to subcellular fractionation for plasma membrane and internal membrane isolation before immunoblotting with GLUT4, GLUT1, and caveolin-1 antibodies (8). | |||||||||||||||
| |||||||||||||||
|
In the brain, GLUT1, GLUT2 and GLUT5 are expressed predominantly in a cell-specific manner [56-58]. | |||||||||||||||
| |||||||||||||||
|
Notable findings for irradiated tumors as compared to control tumors were high levels of Glut-1 expression (13 of 15 tumors), HK II (9 of 16 tumors), and Ki-67 expression (12 of 13 tumors). | |||||||||||||||
| |||||||||||||||
|
AD patients also characteristically feature a decrease in basal cerebral glucose utilization (CGU) in parietotemporal and posterior cingulate cortex (Fukuyama et al., 1994; Mosconi et al., 2004; Langbaum et al., 2009), altered neurometabolic coupling (Melrose et al., 2009), and reduced levels and activity of the endothelial glucose transporter 1 (GLUT-1) that delivers glucose to the brain from the blood (Kalaria and Harik, 1989; Simpson et al., 1994). | |||||||||||||||
| |||||||||||||||
|
General Comments
This test has worked.