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PMID |
Sentence |
1 |
15383720
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Transporters GLUT2 and GLUT4 were expressed in over 90% podocytes.
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2 |
15383720
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Of the GLUT2- and GLUT4-expressing cells, approximately one-fourth expressed the membrane-bound fraction.
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3 |
15383720
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We conclude that cultured rat podocytes possess a differentiated glucose transport system consisting chiefly of facilitative GLUT2 and GLUT4 transporters.
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4 |
15383720
|
Transporters GLUT2 and GLUT4 were expressed in over 90% podocytes.
|
5 |
15383720
|
Of the GLUT2- and GLUT4-expressing cells, approximately one-fourth expressed the membrane-bound fraction.
|
6 |
15383720
|
We conclude that cultured rat podocytes possess a differentiated glucose transport system consisting chiefly of facilitative GLUT2 and GLUT4 transporters.
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7 |
15383720
|
Transporters GLUT2 and GLUT4 were expressed in over 90% podocytes.
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8 |
15383720
|
Of the GLUT2- and GLUT4-expressing cells, approximately one-fourth expressed the membrane-bound fraction.
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9 |
15383720
|
We conclude that cultured rat podocytes possess a differentiated glucose transport system consisting chiefly of facilitative GLUT2 and GLUT4 transporters.
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10 |
29686650
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At the cellular level, the mechanisms leading to the development of insulin resistance include mutations in the insulin receptor gene, impairments in the phosphoinositide 3-kinase (PI3K)/AKT signaling pathway, or perturbations in the trafficking of glucose transporters (GLUTs), which mediate the uptake of glucose into cells.
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11 |
29686650
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Podocytes express several GLUTs, including GLUT1, GLUT2, GLUT3, GLUT4, and GLUT8.
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12 |
29686650
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Of these, the most studied ones are GLUT1 and GLUT4, both shown to be insulin responsive in podocytes.
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13 |
29686650
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After insulin stimulation, GLUT4 is sorted into GLUT4-containing vesicles (GCVs) that translocate to the plasma membrane.
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14 |
29686650
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Studies have revealed novel molecular regulators of the GLUT trafficking in podocytes and unraveled unexpected roles for GLUT1 and GLUT4 in the development of DKD, summarized in this review.
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15 |
30087656
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In this study we investigated the capacity of AngII to modulate glucose uptake in mouse podocytes expressing the human AT1 receptor (AT1R+) after 5 days of exposure to normal (NG, 5.6 mmol/L) or to high (HG, 30 mmol/L) glucose.
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16 |
30087656
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In podocytes cultured under NG conditions, AngII inhibited insulin-stimulated glucose uptake.
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17 |
30087656
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Regardless of the presence or absence of AngII, no effect of insulin on glucose uptake was observed in HG cells.
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18 |
30087656
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Stimulation of glucose transport by AngII was mediated by protein kinase C and by phosphoinositide 3-kinase.
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19 |
30087656
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Glucose dependent surface expression of the glucose transporters GLUT1, GLUT2, and GLUT4 was modulated by AngII in a time and glucose concentration dependent manner.
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20 |
30087656
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Furthermore, despite its inhibitory effect on insulin's action, AngII elevated the number of podocyte insulin receptors in both NG and HG cultured cells.
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21 |
30087656
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These findings demonstrate that AngII modulates podocyte basal, as well as insulin-dependent glucose uptake by regulating glucose transporters and insulin signaling.
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