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Osmotic water transport with glucose in GLUT2 and SGLT.

Naftalin RJ - Biophys. J. (2008)

Bottom Line: Inhibiting glucose exit with phloretin reestablishes vestibular hypertonicity, as it reequilibrates with the cytosolic glucose and net water inflow recommences.Simulated Na(+)-glucose cotransport demonstrates that active glucose accumulation within the vestibule generates water flows simultaneously with the onset of glucose flow and before any flow external to the transporter caused by hypertonicity in the outer cytosolic layers.The molar ratio of water/glucose flow is seen now to relate to the ratio of hydraulic and glucose permeability rather than to water storage capacity of putative water carriers.

View Article: PubMed Central - PubMed

Affiliation: King's College London, Physiology, Waterloo Campus, London SE1 9HN, United Kingdom. richard.naftalin@kcl.ac.uk

ABSTRACT
Carrier-mediated water cotransport is currently a favored explanation for water movement against an osmotic gradient. The vestibule within the central pore of Na(+)-dependent cotransporters or GLUT2 provides the necessary precondition for an osmotic mechanism, explaining this phenomenon without carriers. Simulating equilibrative glucose inflow via the narrow external orifice of GLUT2 raises vestibular tonicity relative to the external solution. Vestibular hypertonicity causes osmotic water inflow, which raises vestibular hydrostatic pressure and forces water, salt, and glucose into the outer cytosolic layer via its wide endofacial exit. Glucose uptake via GLUT2 also raises oocyte tonicity. Glucose exit from preloaded cells depletes the vestibule of glucose, making it hypotonic and thereby inducing water efflux. Inhibiting glucose exit with phloretin reestablishes vestibular hypertonicity, as it reequilibrates with the cytosolic glucose and net water inflow recommences. Simulated Na(+)-glucose cotransport demonstrates that active glucose accumulation within the vestibule generates water flows simultaneously with the onset of glucose flow and before any flow external to the transporter caused by hypertonicity in the outer cytosolic layers. The molar ratio of water/glucose flow is seen now to relate to the ratio of hydraulic and glucose permeability rather than to water storage capacity of putative water carriers.

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Simulation of effects of 1 mM 3-O methyl D-glucose (3-OMG) and 20 mM urea and phloridzin on water flows into oocytes expressing SGLT1. (A) The simulated oocyte percentage volume change (solid line) superimposed on the observed experimental data obtained from Zeuthen et al. (23) (open circles). The first period starts upon exposure to isotonic 1 mM 3-OMG, the second upon addition of 20 mM hypertonic urea + 1 mM 3-OMG, the third upon removal of urea, the fourth upon isotonic removal of 3-OMG and addition of phloridzin (negligible tonicity), and the fifth period upon addition of 20 mM hypertonic urea + phloridzin. (B) The changes in compartmental 3-OMG during the five experimental periods shown in A. (C) The compartmental and extracellular changes in total osmolarity. (D) The separate water flow rates via the transporter, the membrane, and the total transmembrane flows. (E) The changes in vestibular and unstirred layer total osmolarity mOsm, superimposed on the water flow rates via the transporter and membrane using a 100× faster time base than in A and D.
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fig3: Simulation of effects of 1 mM 3-O methyl D-glucose (3-OMG) and 20 mM urea and phloridzin on water flows into oocytes expressing SGLT1. (A) The simulated oocyte percentage volume change (solid line) superimposed on the observed experimental data obtained from Zeuthen et al. (23) (open circles). The first period starts upon exposure to isotonic 1 mM 3-OMG, the second upon addition of 20 mM hypertonic urea + 1 mM 3-OMG, the third upon removal of urea, the fourth upon isotonic removal of 3-OMG and addition of phloridzin (negligible tonicity), and the fifth period upon addition of 20 mM hypertonic urea + phloridzin. (B) The changes in compartmental 3-OMG during the five experimental periods shown in A. (C) The compartmental and extracellular changes in total osmolarity. (D) The separate water flow rates via the transporter, the membrane, and the total transmembrane flows. (E) The changes in vestibular and unstirred layer total osmolarity mOsm, superimposed on the water flow rates via the transporter and membrane using a 100× faster time base than in A and D.

Mentions: Sensitivity table for simulation of water flows in oocytes expressing SGLT (23), as shown in Fig. 3


Osmotic water transport with glucose in GLUT2 and SGLT.

Naftalin RJ - Biophys. J. (2008)

Simulation of effects of 1 mM 3-O methyl D-glucose (3-OMG) and 20 mM urea and phloridzin on water flows into oocytes expressing SGLT1. (A) The simulated oocyte percentage volume change (solid line) superimposed on the observed experimental data obtained from Zeuthen et al. (23) (open circles). The first period starts upon exposure to isotonic 1 mM 3-OMG, the second upon addition of 20 mM hypertonic urea + 1 mM 3-OMG, the third upon removal of urea, the fourth upon isotonic removal of 3-OMG and addition of phloridzin (negligible tonicity), and the fifth period upon addition of 20 mM hypertonic urea + phloridzin. (B) The changes in compartmental 3-OMG during the five experimental periods shown in A. (C) The compartmental and extracellular changes in total osmolarity. (D) The separate water flow rates via the transporter, the membrane, and the total transmembrane flows. (E) The changes in vestibular and unstirred layer total osmolarity mOsm, superimposed on the water flow rates via the transporter and membrane using a 100× faster time base than in A and D.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC2367205&req=5

fig3: Simulation of effects of 1 mM 3-O methyl D-glucose (3-OMG) and 20 mM urea and phloridzin on water flows into oocytes expressing SGLT1. (A) The simulated oocyte percentage volume change (solid line) superimposed on the observed experimental data obtained from Zeuthen et al. (23) (open circles). The first period starts upon exposure to isotonic 1 mM 3-OMG, the second upon addition of 20 mM hypertonic urea + 1 mM 3-OMG, the third upon removal of urea, the fourth upon isotonic removal of 3-OMG and addition of phloridzin (negligible tonicity), and the fifth period upon addition of 20 mM hypertonic urea + phloridzin. (B) The changes in compartmental 3-OMG during the five experimental periods shown in A. (C) The compartmental and extracellular changes in total osmolarity. (D) The separate water flow rates via the transporter, the membrane, and the total transmembrane flows. (E) The changes in vestibular and unstirred layer total osmolarity mOsm, superimposed on the water flow rates via the transporter and membrane using a 100× faster time base than in A and D.
Mentions: Sensitivity table for simulation of water flows in oocytes expressing SGLT (23), as shown in Fig. 3

Bottom Line: Inhibiting glucose exit with phloretin reestablishes vestibular hypertonicity, as it reequilibrates with the cytosolic glucose and net water inflow recommences.Simulated Na(+)-glucose cotransport demonstrates that active glucose accumulation within the vestibule generates water flows simultaneously with the onset of glucose flow and before any flow external to the transporter caused by hypertonicity in the outer cytosolic layers.The molar ratio of water/glucose flow is seen now to relate to the ratio of hydraulic and glucose permeability rather than to water storage capacity of putative water carriers.

View Article: PubMed Central - PubMed

Affiliation: King's College London, Physiology, Waterloo Campus, London SE1 9HN, United Kingdom. richard.naftalin@kcl.ac.uk

ABSTRACT
Carrier-mediated water cotransport is currently a favored explanation for water movement against an osmotic gradient. The vestibule within the central pore of Na(+)-dependent cotransporters or GLUT2 provides the necessary precondition for an osmotic mechanism, explaining this phenomenon without carriers. Simulating equilibrative glucose inflow via the narrow external orifice of GLUT2 raises vestibular tonicity relative to the external solution. Vestibular hypertonicity causes osmotic water inflow, which raises vestibular hydrostatic pressure and forces water, salt, and glucose into the outer cytosolic layer via its wide endofacial exit. Glucose uptake via GLUT2 also raises oocyte tonicity. Glucose exit from preloaded cells depletes the vestibule of glucose, making it hypotonic and thereby inducing water efflux. Inhibiting glucose exit with phloretin reestablishes vestibular hypertonicity, as it reequilibrates with the cytosolic glucose and net water inflow recommences. Simulated Na(+)-glucose cotransport demonstrates that active glucose accumulation within the vestibule generates water flows simultaneously with the onset of glucose flow and before any flow external to the transporter caused by hypertonicity in the outer cytosolic layers. The molar ratio of water/glucose flow is seen now to relate to the ratio of hydraulic and glucose permeability rather than to water storage capacity of putative water carriers.

Show MeSH
Related in: MedlinePlus