Use of phlorizin binding to demonstrate induction of intestinal glucose transporters.
We used specific binding of phlorizin to the intact intestinal mucosa in order to measure glucose transport site density in intestines of mice fed a high-carbohydrate or no-carbohydrate diet. Nonspecific binding varied with intestinal position but showed only modest dependence on diet. Specific binding to glucose transporters was 1.9 times greater in jejunum of high-carbohydrate mice than of no-carbohydrate mice; this ratio was the same as the ratio for Vmax values of active D-glucose uptake between the two diet groups. The gradient in specific binding of phlorizin along the intestine paralleled the gradient in Vmax of glucose transport. These results directly demonstrate that the increase in intestinal glucose transport caused by a high-carbohydrate diet is due to induction of glucose transporters. They also indicate that the normal positional gradient in glucose transport along the intestine arises from a gradient in transporters, induced by the normal gradient in luminal glucose concentration.
D000818:Animals; D004040:Dietary Carbohydrates / Q000494:pharmacology; D004044:Dietary Proteins / Q000494:pharmacology; D005947:Glucose / Q000378:metabolism; D066298:In Vitro Techniques; D007413:Intestinal Mucosa / Q000187:drug effects / Q000378:metabolism*; D007583:Jejunum / Q000187:drug effects / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D051379:Mice; D009004:Monosaccharide Transport Proteins / Q000378:metabolism*; D010695:Phlorhizin / Q000378:metabolism*; D011485:Protein Binding
D004040:Dietary Carbohydrates; D004044:Dietary Proteins; D009004:Monosaccharide Transport Proteins; D010695:Phlorhizin; D005947:Glucose