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Endosomal SGLT1 and its possible role in the regulation of D-glucose uptake

MPG-Autoren

Khoursandi,  Saeed
Max Planck Institute of Molecular Physiology, Max Planck Society;

Scharlau,  Daniel
Max Planck Institute of Molecular Physiology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons98705

Kinne,  Rolf K. H.
Sonstige Wissenschaftliche Organisationseinheiten, Max Planck Institute of Molecular Physiology, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons98706

Kipp,  Helmut
Sonstige Wissenschaftliche Organisationseinheiten, Max Planck Institute of Molecular Physiology, Max Planck Society;

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Zitation

Khoursandi, S., Scharlau, D., Kinne, R. K. H., & Kipp, H. (2004). Endosomal SGLT1 and its possible role in the regulation of D-glucose uptake.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0014-0B89-3
Zusammenfassung
To elucidate the role of endosomal SGLTl in the regulation of sodium-dependent D-glucose uptake into enterocytes, we investigated the relationship between subcellular distribution of SGLTl and sodium-dependent 14C-methylglucose uptake into Caco-2 cells under varying conditions. Incubation with mastoparan shifted a large amount of SGLTl from the apical membrane to intracellular sites and significantly reduced sodiumdependent 14C-methylglucose uptake. We also investigated the effect of extracellular D-glucose levels. Cells pre-incubated with D-glucose free medium exhibited a significantly higher sodiumdependent 14C-methylglucose uptake than cells pre-incubated with high D-glucose medium. No difference in the overall subcellular distribution of SGLTl was observed between the two conditions. Interestingly, the change in 14C-methylglucose uptake was attenuated when microtubules were depolymerized. These results suggest that pharmacologically, D-glucose uptake can be regulated by a shift of the steady state distribution of carriers from the plasma membrane to endosomes. The physiological substrate D-glucose alters substrate uptake by an additional mechanism that requires microtubule-dependent vesicle transport without a change in the steady state distribution. This phenomenon could be explained by the hypothesis that SGLTl undergoes an activation/deactivation cycle during its constitutive cycling from endosomes to the plasma membrane and back.