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World J Gastroenterol. Mar 7, 2008; 14(9): 1365-1369
Published online Mar 7, 2008. doi: 10.3748/wjg.14.1365
Absence of Na+/sugar cotransport activity in Barrett’s metaplasia
Lisa J Murray, Owen Tully, David S Rudolph, Marysue Whitby, Mary C Valenzano, Giancarlo Mercogliano, James J Thornton, James M Mullin
Lisa J Murray, Marysue Whitby, Mary C Valenzano, James M Mullin, Lankenau Institute for Medical Research, Wynnewood, PA, United States
Owen Tully, David S Rudolph, Lankenau Hospital, Department of Medicine, Wynnewood, PA 19096, United States
Giancarlo Mercogliano, James J Thornton, James M Mullin, Lankeanu Hospital, Division of Gastroenterology, Wynnewood, PA 19096, United States
Lisa J Murray, Saint Joseph’s University, Department of Biology, Philadelphia, PA 19096, United States
Correspondence to: James M Mullin, PhD, Lankenau Institute for Medical Research, 100 Lancaster Avenue, Wynnewood, PA 19096, United States. mullinj@mlhs.org
Telephone: +1-610-6452703
Fax: +1-610-6452205
Received: August 3, 2007
Revised: January 1, 2008
Published online: March 7, 2008
Abstract

AIM: 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°C. 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/&mgr;g 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.

CONCLUSION: Despite the intestinal enterocyte phenotype of BE, Na+-dependent, sugar transport activity is not present in these cells.

Keywords: Barrett’s esophagus; Cancer; Biomarker; Sodium glucose cotransporters; Glucose transport; Alpha-methyl-D-glucoside; Phlorizin; Esophagus; Metaplasia