Absence of Na^+/sugar cotransport activity in Barrett's metaplasia  

作　　者：Lisa J Murray Owen Tully David S Rudolph Marysue Whitby Mary C Valenzano Giancarlo Mercogliano James J Thornton James M Mullin 

机构地区：[1]Lankenau Institute for Medical Research,Wynnewood,PA,United States Saint Joseph's University,Department of Biology,Philadelphia,PA 19096,United States [2]Lankenau Hospital, Department of Medicine, Wynnewood,PA 19096,United States [3]Lankenau Hospital, Department of Medicine,Wynnewood,PA 19096, United States [4]Lankenau Institute for Medical Research,Wynnewood,PA,United States [5]Lankeanu Hospital,Division of Gastroenterology,Wynnewood, PA 19096,United States [6]Lankeanu Hospital,Division of Gastroenterology,Wynnewood,PA 19096,United States

出　　处：《World Journal of Gastroenterology》2008年第9期1365-1369,共5页世界胃肠病学杂志（英文版）

基　　金：The Oncologic Foundation of Buffalo, the Sharpe-Strumia fund, and the Pennsylvania Department of Health

摘　　要：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℃. 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/μg 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 nosignificant 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.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 nonmetabolizable 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℃. 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/μg 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 nosignificant 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.

关 键 词：Barrett＇s esophagus Cancer Biomarker Sodium glucose cotransporters Glucose transport Alphamethyl-D-glucoside PHLORIZIN ESOPHAGUS METAPLASIA 

分 类 号：R571[医药卫生—消化系统]