title: Inhibition of glucose absorption by phlorizin affects intestinal functions in rats.
abstract: BACKGROUND
  To investigate the mechanism of regulation of intestinal disaccharidase activity and glucose absorption, the effect of dietary intake of phlorizin, a potent and specific inhibitor of intestinal glucose transport, on intestinal disaccharidase activity and Na(+)-dependent glucose transporter was examined in rats.
  
  
  METHODS
  Jejunal disaccharidase activity and the number of Na(+)-dependent glucose transporters were determined in rats maintained on a low-starch diet, a high-starch diet, or low-starch diets containing various amounts of phlorizin (0.1%-0.9% wt/wt).
  
  
  RESULTS
  Jejunal disaccharidase activity increased in a dose- and time-dependent manner. Stimulation of jejunal disaccharidase activity only occurred when phlorizin was added to starch-containing diets, not when it was added to a carbohydrate-free diet. Addition of the same amount of phloretin and glucose (constituents of phlorizin), to the diet failed to increase disaccharidase activity. The maximum binding of phlorizin to brush border membrane vesicles was increased in the rats fed phlorizin, whereas the dissociation constant remained unchanged, suggesting an increase of glucose transporter expression.
  
  
  CONCLUSIONS
  Dietary phlorizin increased the jejunal disaccharidase activity and Na(+)-dependent glucose transporter expression. The trigger for these changes may have been due to an increased luminal glucose content.
authors.affiliation: Department of Nutrition, School of Medicine, University of Tokushima, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Minami
authors.forename: J R
authors.initials: JR
authors.lastname: Kim
authors.forename: K
authors.initials: K
authors.lastname: Tada
authors.forename: F
authors.initials: F
authors.lastname: Takahashi
authors.forename: K
authors.initials: K
authors.lastname: Miyamoto
authors.forename: Y
authors.initials: Y
authors.lastname: Nakabou
authors.forename: K
authors.initials: K
authors.lastname: Sakai
authors.forename: H
authors.initials: H
authors.lastname: Hagihira
mesh_terms: D000284:Administration, Oral; D000704:Analysis of Variance; D000818:Animals; D004040:Dietary Carbohydrates; D004187:Disaccharides / Q000378:metabolism; D004305:Dose-Response Relationship, Drug; D005947:Glucose / Q000008:administration & dosage / Q000032:analysis / Q000493:pharmacokinetics*; D007408:Intestinal Absorption / Q000187:drug effects / Q000502:physiology*; D007422:Intestines / Q000201:enzymology / Q000502:physiology*; D007425:Intracellular Membranes / Q000378:metabolism; D007583:Jejunum / Q000201:enzymology / Q000502:physiology / Q000648:ultrastructure; D008297:Male; D008871:Microvilli / Q000201:enzymology / Q000502:physiology / Q000648:ultrastructure; D009004:Monosaccharide Transport Proteins / Q000502:physiology; D010695:Phlorhizin / Q000008:administration & dosage / Q000378:metabolism / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012964:Sodium / Q000502:physiology; D013393:Sucrase / Q000378:metabolism / Q000502:physiology; D013997:Time Factors
chemical_list: D004040:Dietary Carbohydrates; D004187:Disaccharides; D009004:Monosaccharide Transport Proteins; D012964:Sodium; D010695:Phlorhizin; D013393:Sucrase; D005947:Glucose