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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 the changes in the molar ratio of water/3-OMG inflow via Glut2. The lines shown indicate the effects of changing the parameter values of the transporter Pw12 on inflow phase 1 and outflow phase 2 with varying values of the hydraulic permeability.
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fig4: Simulation of the changes in the molar ratio of water/3-OMG inflow via Glut2. The lines shown indicate the effects of changing the parameter values of the transporter Pw12 on inflow phase 1 and outflow phase 2 with varying values of the hydraulic permeability.

Mentions: In the simulations shown here, GLUT2 vestibular hypertonicity generated by 3-OMG inflow increases the water/3-OMG flow ratios, and hypotonicity during 3-OMG exit decreases the ratio (Table 1 and Figs. 2 F and 4). The estimated molar ratio of water/3-OMG climbs from 20 to 180 during 3-OMG inflow and abruptly decreases during exit to 20 and returns to 35. These findings differ from those of Zeuthen et al. for GLUT2 (7,9). Most of these differences can be ascribed to uncertainties regarding initial rates of 3-OMG exit and uptake as monitored by isotope flow. This is illustrated by the relatively high sensitivity of the apparent stoichiometry of water/glucose flow during net exit (Table 1) to alteration in the rate of mixing, k, in external solution.


Osmotic water transport with glucose in GLUT2 and SGLT.

Naftalin RJ - Biophys. J. (2008)

Simulation of the changes in the molar ratio of water/3-OMG inflow via Glut2. The lines shown indicate the effects of changing the parameter values of the transporter Pw12 on inflow phase 1 and outflow phase 2 with varying values of the hydraulic permeability.
© Copyright Policy
Related In: Results  -  Collection

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

fig4: Simulation of the changes in the molar ratio of water/3-OMG inflow via Glut2. The lines shown indicate the effects of changing the parameter values of the transporter Pw12 on inflow phase 1 and outflow phase 2 with varying values of the hydraulic permeability.
Mentions: In the simulations shown here, GLUT2 vestibular hypertonicity generated by 3-OMG inflow increases the water/3-OMG flow ratios, and hypotonicity during 3-OMG exit decreases the ratio (Table 1 and Figs. 2 F and 4). The estimated molar ratio of water/3-OMG climbs from 20 to 180 during 3-OMG inflow and abruptly decreases during exit to 20 and returns to 35. These findings differ from those of Zeuthen et al. for GLUT2 (7,9). Most of these differences can be ascribed to uncertainties regarding initial rates of 3-OMG exit and uptake as monitored by isotope flow. This is illustrated by the relatively high sensitivity of the apparent stoichiometry of water/glucose flow during net exit (Table 1) to alteration in the rate of mixing, k, in external solution.

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