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.
基金
The Oncologic Foundation of Buffalo, the Sharpe-Strumia fund, and the Pennsylvania Department of Health
关键词
巴雷特组织转化
癌症
钠离子/葡萄糖协同运输
根皮苷
Barrett＇s esophagus
Cancer
Biomarker
Sodium glucose cotransporters
Glucose transport
Alphamethyl-D-glucoside
Phlorizin
Esophagus
Metaplasia
