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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Short-chain glucose polymer and anthracene-9-carboxylic acid inhibit water and electrolyte secretion induced by dibutyryl cyclic AMP in the small intestine.

Glucose-stimulated sodium absorption is the rationale for treatment with glucose-based oral rehydration solution in diarrhea. Concurrent treatment with pharmacological inhibitors, which specifically block chloride secretion, may be a useful adjunct to oral fluid therapy. To examine this hypothesis, the authors determined the intestinal water and ion transport rates in rat small intestine during the secretory phase induced by perfusion with N6-2'-0-dibutyryl adenosine 3',5'-cyclic monophosphate (dbcAMP), 1.0 mmol/L. A marker (polyethylene glycol 4000) dilution technique was used to evaluate the antisecretory effects of a defined short-chain glucose polymer, D-glucose, and a chloride channel blocker, anthracene-9-carboxylic acid (A-9-C). The results showed that dbcAMP induced small intestinal water and chloride ion secretion rapidly and reliably. The 2.5% concentration of rice short glucose polymer (G2, 22.7%; G3, 28.2%; G4, 14.0%; G5, 16.6%; G6, 11.6%; G7-9, 6.9%) is a better carbohydrate than the 2.5% concentration of D-glucose in reversing secretion of water, chloride, and sodium ions induced by dbcAMP. The combination of A-9-C and the glucose polymer can reverse dbcAMP-induced intestinal secretion and produces significantly (P less than 0.05) better antisecretory effect on water, sodium, and chloride ions than D-glucose with A-9-C.[1]


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