A hydrolase-related transport system is not required to explain the intestinal uptake of glucose liberated from phlorizin |
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Authors: | Dean A Warden Franklin F Fannin James O Evans Dan W Hanke Donald F Diedrich |
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Institution: | Department of Pharmacology, University of Kentucky Medical Center, Lexington, KY 40536 U.S.A. |
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Abstract: | The fate of 3H]glucose released from a wide range of 3H]phlorizin concentrations by phlorizin hydrolase has been studied under conditions where the Na+-dependent glucose transport system in hamster intestine is profoundly inhibited by the glucoside. At 0.2–2.0 mM phlorizin, the 3H]glucose uptake was a constant 11–12% of that generated by the enzyme and at the highest level, it was reduced to that of passive diffusion. Glucose liberated from 0.2 mM 3H]phlorizin is accumulated at a rate nearly equal to that found for 0.2 mM 14C]glucose when this free sugar uptake is measured in a medium containing 0.2 mM unlabeled phlorizin. Furthermore, without sodium, the accumulation rates of hydrolase-derived or exogenous glucose are both reduced to the rate of 14C]mannitol. Our results indicate that the glucose released from phlorizin enters the tissue via the small fraction of the Na+-dependent glucose carriers which escape phlorizin blockade together with a mannitol-like passive diffusion. It enjoys a kinetic advantage for tissue entry over free glucose in the medium by virtue of the position of the site where it is formed, i.e. inside the unstirred water layer and near normal entry portals. No special hydrolase-related transport system, like the one proposed for disaccharides, needs to be considered to account for our findings. |
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Keywords: | Glucose uptake Phlorizin Hydrolase Intestinal transport Disaccharidase |
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