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 

作者机构：Lankenau Institute for Medical ResearchWynnewoodPAUnited States Saint Joseph's UniversityDepartment of BiologyPhiladelphiaPA 19096United States Lankenau Hospital Department of Medicine WynnewoodPA 19096United States Lankenau Hospital Department of MedicineWynnewoodPA 19096 United States Lankenau Institute for Medical ResearchWynnewoodPAUnited States Lankeanu HospitalDivision of GastroenterologyWynnewood PA 19096United States Lankeanu HospitalDivision of GastroenterologyWynnewoodPA 19096United States 

出 版 物：《World Journal of Gastroenterology》 (世界胃肠病学杂志（英文版）)

年 卷 期：2008年第14卷第9期

页      面：1365-1369页

核心收录：

学科分类：1002[医学-临床医学] 100201[医学-内科学(含：心血管病、血液病、呼吸系病、消化系病、内分泌与代谢病、肾病、风湿病、传染病)] 10[医学] 

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

主　　题：Barrett's esophagus Cancer Biomarker Sodium glucose cotransporters Glucose transport Alphamethyl-D-glucoside Phlorizin Esophagus Metaplasia 

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.