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2-Deoxy-D-glucose transport in dog kidney
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| Zeitschriftentitel: | American Journal of Physiology-Renal Physiology |
|---|---|
| Personen und Körperschaften: | , |
| In: | American Journal of Physiology-Renal Physiology, 242, 1982, 6, S. F711-F720 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
American Physiological Society
|
| Schlagwörter: |
| author_facet |
Silverman, M. Turner, R. J. Silverman, M. Turner, R. J. |
|---|---|
| author |
Silverman, M. Turner, R. J. |
| spellingShingle |
Silverman, M. Turner, R. J. American Journal of Physiology-Renal Physiology 2-Deoxy-D-glucose transport in dog kidney Physiology |
| author_sort |
silverman, m. |
| spelling |
Silverman, M. Turner, R. J. 1931-857X 1522-1466 American Physiological Society Physiology http://dx.doi.org/10.1152/ajprenal.1982.242.6.f711 <jats:p> Osmotically active brush border membrane (BBM) and antiluminal membrane (ALM) vesicles prepared from dog kidney cortex were used to investigate transport of 2-deoxy-D-glucose (2DG). A parallel in vivo study was carried out using the pulse-injection multiple indicator-dilution technique. Single-pass indicator-dilution experiments demonstrate both luminal and antiluminal interactions for 2DG. The antiluminal interaction is blocked by large systemic doses of phlorizin (100-200 mg/kg). With plasma glucose concentration in the range of 4-5 mM fractional luminal extraction of 2-[14C]DG relative to simultaneously filtered creatinine is 25 +/- 2%. This luminal extraction can be inhibited by raising plasma glucose concentration to approximately 30 mM and by administration of low systemic doses of phlorizin (6-8 mg/Kg). 2DG uptake into BBM vesicles equilibrates into the same intravesicular volume as D-glucose. A definite Na+ component of 2DG uptake can be defined which is more sensitive to inhibition by phlorizin than by phloretin and is also inhibited by D-glucose and alpha-methyl-D-glucoside but not by L-glucose. But compared with D-glucose, the Na+-dependent BBM uptake of 2DG is greatly reduced. 2DG uptake into ALM vesicles is independent of Na+, is more sensitive to inhibition by phloretin than by phlorizin, and is also blocked by cytochalasin B but not by alpha-methyl-D-glucoside. Influx of 2-[14C] DG into ALM vesicles is increased by preloading with unlabeled D-glucose. Conversely influx of D[14C]glucose into ALM vesicles is accelerated by preloading with unlabeled 2DG. ALM influx of radiolabeled 2DG is accelerated by D-glucose, 3-O-methyl-D-glucose, D-galactose, and unlabeled 2DG but not by alpha-methyl-D-glucoside. The specificity of inhibition and countertransport results from in vivo and in vitro experiments are consistent with the proposal that 2DG shares a common carrier mechanism with D-glucose at each of the opposing membrane surfaces. </jats:p> 2-Deoxy-D-glucose transport in dog kidney American Journal of Physiology-Renal Physiology |
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10.1152/ajprenal.1982.242.6.f711 |
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American Physiological Society, 1982 |
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American Physiological Society, 1982 |
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1931-857X 1522-1466 |
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1982 |
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American Physiological Society |
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American Journal of Physiology-Renal Physiology |
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49 |
| title |
2-Deoxy-D-glucose transport in dog kidney |
| title_unstemmed |
2-Deoxy-D-glucose transport in dog kidney |
| title_full |
2-Deoxy-D-glucose transport in dog kidney |
| title_fullStr |
2-Deoxy-D-glucose transport in dog kidney |
| title_full_unstemmed |
2-Deoxy-D-glucose transport in dog kidney |
| title_short |
2-Deoxy-D-glucose transport in dog kidney |
| title_sort |
2-deoxy-d-glucose transport in dog kidney |
| topic |
Physiology |
| url |
http://dx.doi.org/10.1152/ajprenal.1982.242.6.f711 |
| publishDate |
1982 |
| physical |
F711-F720 |
| description |
<jats:p> Osmotically active brush border membrane (BBM) and antiluminal membrane (ALM) vesicles prepared from dog kidney cortex were used to investigate transport of 2-deoxy-D-glucose (2DG). A parallel in vivo study was carried out using the pulse-injection multiple indicator-dilution technique. Single-pass indicator-dilution experiments demonstrate both luminal and antiluminal interactions for 2DG. The antiluminal interaction is blocked by large systemic doses of phlorizin (100-200 mg/kg). With plasma glucose concentration in the range of 4-5 mM fractional luminal extraction of 2-[14C]DG relative to simultaneously filtered creatinine is 25 +/- 2%. This luminal extraction can be inhibited by raising plasma glucose concentration to approximately 30 mM and by administration of low systemic doses of phlorizin (6-8 mg/Kg). 2DG uptake into BBM vesicles equilibrates into the same intravesicular volume as D-glucose. A definite Na+ component of 2DG uptake can be defined which is more sensitive to inhibition by phlorizin than by phloretin and is also inhibited by D-glucose and alpha-methyl-D-glucoside but not by L-glucose. But compared with D-glucose, the Na+-dependent BBM uptake of 2DG is greatly reduced. 2DG uptake into ALM vesicles is independent of Na+, is more sensitive to inhibition by phloretin than by phlorizin, and is also blocked by cytochalasin B but not by alpha-methyl-D-glucoside. Influx of 2-[14C] DG into ALM vesicles is increased by preloading with unlabeled D-glucose. Conversely influx of D[14C]glucose into ALM vesicles is accelerated by preloading with unlabeled 2DG. ALM influx of radiolabeled 2DG is accelerated by D-glucose, 3-O-methyl-D-glucose, D-galactose, and unlabeled 2DG but not by alpha-methyl-D-glucoside. The specificity of inhibition and countertransport results from in vivo and in vitro experiments are consistent with the proposal that 2DG shares a common carrier mechanism with D-glucose at each of the opposing membrane surfaces. </jats:p> |
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| description | <jats:p> Osmotically active brush border membrane (BBM) and antiluminal membrane (ALM) vesicles prepared from dog kidney cortex were used to investigate transport of 2-deoxy-D-glucose (2DG). A parallel in vivo study was carried out using the pulse-injection multiple indicator-dilution technique. Single-pass indicator-dilution experiments demonstrate both luminal and antiluminal interactions for 2DG. The antiluminal interaction is blocked by large systemic doses of phlorizin (100-200 mg/kg). With plasma glucose concentration in the range of 4-5 mM fractional luminal extraction of 2-[14C]DG relative to simultaneously filtered creatinine is 25 +/- 2%. This luminal extraction can be inhibited by raising plasma glucose concentration to approximately 30 mM and by administration of low systemic doses of phlorizin (6-8 mg/Kg). 2DG uptake into BBM vesicles equilibrates into the same intravesicular volume as D-glucose. A definite Na+ component of 2DG uptake can be defined which is more sensitive to inhibition by phlorizin than by phloretin and is also inhibited by D-glucose and alpha-methyl-D-glucoside but not by L-glucose. But compared with D-glucose, the Na+-dependent BBM uptake of 2DG is greatly reduced. 2DG uptake into ALM vesicles is independent of Na+, is more sensitive to inhibition by phloretin than by phlorizin, and is also blocked by cytochalasin B but not by alpha-methyl-D-glucoside. Influx of 2-[14C] DG into ALM vesicles is increased by preloading with unlabeled D-glucose. Conversely influx of D[14C]glucose into ALM vesicles is accelerated by preloading with unlabeled 2DG. ALM influx of radiolabeled 2DG is accelerated by D-glucose, 3-O-methyl-D-glucose, D-galactose, and unlabeled 2DG but not by alpha-methyl-D-glucoside. The specificity of inhibition and countertransport results from in vivo and in vitro experiments are consistent with the proposal that 2DG shares a common carrier mechanism with D-glucose at each of the opposing membrane surfaces. </jats:p> |
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| imprint | American Physiological Society, 1982 |
| imprint_str_mv | American Physiological Society, 1982 |
| institution | DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-D161, DE-Gla1, DE-Zi4, DE-15, DE-Pl11, DE-Rs1, DE-14, DE-Ch1 |
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| series | American Journal of Physiology-Renal Physiology |
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| spelling | Silverman, M. Turner, R. J. 1931-857X 1522-1466 American Physiological Society Physiology http://dx.doi.org/10.1152/ajprenal.1982.242.6.f711 <jats:p> Osmotically active brush border membrane (BBM) and antiluminal membrane (ALM) vesicles prepared from dog kidney cortex were used to investigate transport of 2-deoxy-D-glucose (2DG). A parallel in vivo study was carried out using the pulse-injection multiple indicator-dilution technique. Single-pass indicator-dilution experiments demonstrate both luminal and antiluminal interactions for 2DG. The antiluminal interaction is blocked by large systemic doses of phlorizin (100-200 mg/kg). With plasma glucose concentration in the range of 4-5 mM fractional luminal extraction of 2-[14C]DG relative to simultaneously filtered creatinine is 25 +/- 2%. This luminal extraction can be inhibited by raising plasma glucose concentration to approximately 30 mM and by administration of low systemic doses of phlorizin (6-8 mg/Kg). 2DG uptake into BBM vesicles equilibrates into the same intravesicular volume as D-glucose. A definite Na+ component of 2DG uptake can be defined which is more sensitive to inhibition by phlorizin than by phloretin and is also inhibited by D-glucose and alpha-methyl-D-glucoside but not by L-glucose. But compared with D-glucose, the Na+-dependent BBM uptake of 2DG is greatly reduced. 2DG uptake into ALM vesicles is independent of Na+, is more sensitive to inhibition by phloretin than by phlorizin, and is also blocked by cytochalasin B but not by alpha-methyl-D-glucoside. Influx of 2-[14C] DG into ALM vesicles is increased by preloading with unlabeled D-glucose. Conversely influx of D[14C]glucose into ALM vesicles is accelerated by preloading with unlabeled 2DG. ALM influx of radiolabeled 2DG is accelerated by D-glucose, 3-O-methyl-D-glucose, D-galactose, and unlabeled 2DG but not by alpha-methyl-D-glucoside. The specificity of inhibition and countertransport results from in vivo and in vitro experiments are consistent with the proposal that 2DG shares a common carrier mechanism with D-glucose at each of the opposing membrane surfaces. </jats:p> 2-Deoxy-D-glucose transport in dog kidney American Journal of Physiology-Renal Physiology |
| spellingShingle | Silverman, M., Turner, R. J., American Journal of Physiology-Renal Physiology, 2-Deoxy-D-glucose transport in dog kidney, Physiology |
| title | 2-Deoxy-D-glucose transport in dog kidney |
| title_full | 2-Deoxy-D-glucose transport in dog kidney |
| title_fullStr | 2-Deoxy-D-glucose transport in dog kidney |
| title_full_unstemmed | 2-Deoxy-D-glucose transport in dog kidney |
| title_short | 2-Deoxy-D-glucose transport in dog kidney |
| title_sort | 2-deoxy-d-glucose transport in dog kidney |
| title_unstemmed | 2-Deoxy-D-glucose transport in dog kidney |
| topic | Physiology |
| url | http://dx.doi.org/10.1152/ajprenal.1982.242.6.f711 |