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Acute and chronic exposure of rat intestinal mucosa to dextran promotes SGLT1‐mediated glucose transport
Author(s) -
ES Debnam,
EE Denholm,
GK Grimble
Publication year - 1998
Publication title -
european journal of clinical investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.164
H-Index - 107
eISSN - 1365-2362
pISSN - 0014-2972
DOI - 10.1046/j.1365-2362.1998.00352.x
Subject(s) - dextran , phlorizin , maltodextrin , chemistry , glucose uptake , carbohydrate , glucose transporter , medicine , brush border , hydrolysis , vesicle , sugar , endocrinology , biochemistry , chromatography , insulin , biology , membrane , spray drying
Background The intestinal handling of dextran, an α‐1,6‐linked glucose polymer, is poor compared with starch, and some ingested dextran might therefore reach the lower small intestine. As luminal sugar up‐regulates SGLT1 (sodium‐dependent glucose transporter) locally, we report the effects of a dextran‐enriched diet on jejunal and ileal brush border membrane (BBM) glucose uptake. Methods Rats were maintained on a diet containing 65% maltodextrin or 32.5% maltodextrin + 32.5% dextran (10 kD or 40 kD) for 8–10 days, and the kinetics of phlorizin‐sensitive [ 3 H]‐glucose uptake by purified BBM vesicles was determined. Results Ingestion of 40‐kD but not 10‐kD dextran increased V max for jejunal and ileal glucose uptake (+64.3% and +61.8% respectively, both P < 0.02). The transport response to 40‐kD dextran was in keeping with lower levels of expired H 2 at the end of the feeding period. High‐performance liquid chromatography (HPLC) analysis of luminal contents indicated extensive hydrolysis of ingested dextran. Finally, 3‐h jejunal exposure to 40‐kD dextran in vivo increased the V max for glucose uptake by jejunal BBM. Conclusion It is likely that increased SGLT1‐mediated glucose uptake after short or longer term mucosal exposure to dextran results from luminal dextran per se or a hydrolysis product. The clinical implications of this up‐regulation are discussed.