title: Absence of Na+/sugar cotransport activity in Barrett's metaplasia.
abstract: OBJECTIVE
  To evaluate the presence of Na+-dependent, active, sugar transport in Barrett's epithelia as an intestinal biomarker, based on the well-documented, morphological intestinal phenotype of Barrett's esophagus (BE).
  
  
  METHODS
  We examined uptake of the nonmeta-bolizable glucose analogue, alpha-methyl-D-glucoside (AMG), a substrate for the entire sodium glucose cotransporter (SGLT) family of transport proteins. During upper endoscopy, patients with BE or with uncomplicated gastroesophageal reflux disease (GERD) allowed for duodenal, gastric fundic, and esophageal mucosal biopsies to be taken. Biopsies were incubated in bicarbonate-buffered saline (KRB) containing 0.1 mmol/L 14C-AMG for 60 min at 20 centigrade. Characterized by abundant SGLT, duodenum served as a positive control while gastric fundus and normal esophagus, known to lack SGLT, served as negative controls.
  
  
  RESULTS
  Duodenal biopsies accumulated 249.84+/-35.49 (SEM) picomoles AMG/microg DNA (n=12), gastric fundus biopsies 36.20+/-6.62 (n=12), normal esophagus 12.10+/-0.59 (n=3) and Barrett's metaplasia 29.79+/-5.77 (n=8). There was a statistical difference (P<0.01) between biopsies from duodenum and each other biopsy site but there was no statistically significant difference between normal esophagus and BE biopsies. 0.5 mmol/L phlorizin (PZ) inhibited AMG uptake into duodenal mucosa by over 89%, but had no significant effect on AMG uptake into gastric fundus, normal esophagus, or Barrett's tissue. In the absence of Na+ (all Na+ salts replaced by Li+ salts), AMG uptake in duodenum was decreased by over 90%, while uptake into gastric, esophageal or Barrett's tissue was statistically unaffected.
  
  
  CONCLUSIONS
  Despite the intestinal enterocyte phenotype of BE, Na+-dependent, sugar transport activity is not present in these cells.
authors.affiliation: Lankenau Institute for Medical Research, 100 Lancaster Avenue, Wynnewood, PA 19096, United States.
authors.forename: Lisa J
authors.initials: LJ
authors.lastname: Murray
authors.forename: Owen
authors.initials: O
authors.lastname: Tully
authors.forename: David S
authors.initials: DS
authors.lastname: Rudolph
authors.forename: Marysue
authors.initials: M
authors.lastname: Whitby
authors.forename: Mary C
authors.initials: MC
authors.lastname: Valenzano
authors.forename: Giancarlo
authors.initials: G
authors.lastname: Mercogliano
authors.forename: James J
authors.initials: JJ
authors.lastname: Thornton
authors.forename: James M
authors.initials: JM
authors.lastname: Mullin
mesh_terms: D000368:Aged; D000369:Aged, 80 and over; D001471:Barrett Esophagus / Q000378:metabolism* / Q000473:pathology; D001692:Biological Transport; D015415:Biomarkers / Q000378:metabolism; D001706:Biopsy; D016022:Case-Control Studies; D004386:Duodenum / Q000378:metabolism / Q000473:pathology; D004947:Esophagus / Q000378:metabolism* / Q000473:pathology; D005260:Female; D005748:Gastric Fundus / Q000378:metabolism / Q000473:pathology; D006801:Humans; D008297:Male; D008757:Methylglucosides / Q000378:metabolism; D008875:Middle Aged; D010641:Phenotype; D051247:Sodium-Glucose Transport Proteins / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D008757:Methylglucosides; D051247:Sodium-Glucose Transport Proteins; C027020:methylglucoside