1006 Combination of Laparoscopy and Enhanced Recovery Program Improves Outcomes After Ileocecal Resection for Crohn's Disease

Activation of sweet taste receptors may enhance glucose uptake several fold in rat intestine. AIM: To explore mechanisms of sweet taste receptor activation in glucose uptake in 3 intestinal cell lines. HYPOTHESIS: The artificial sweetener, acesulfame potassium (AceK), increases glucose uptake via activating sweet taste receptors to induce translocation GLUT2 to the apical membrane through the PLC βII pathway. METHODS: Caco-2, RIE-1, and IEC-6 cells (human, rat, and rat intestinal cell lines) were seeded on a 24-well plate at a density of 4x104 cells/cm2 in growth culture media and left to differentiate for 15 days after confluence. Caco-2 and RIE-1 cells express GLUT2, while IEC-6 cells do not. Cells were starved from glucose for 1 h and pre-incubated with and without 10 mM AceK for 30 min. Glucose uptake was measured by incubating the cells for 1 to 10 min with 0.5-50 mM glucose with and without 10 mM AceK. 14C-D-glucose was used to measure stereospecific, transporter-mediated uptake and 3H-L-glucose to measure passive uptake with or without the inhibitors 10 μM U-73122, a PLC βII inhibitor, 10 μM chelerythrine, a PKC inhibitor, and 2 μM cytochalasin B, a microtubular system disrupter. Glucose uptake was stopped by adding ice-cold PBS; cells were washed with PBS 2 times and solubilized with 0.1 N NaOH. All experiments were done on at least 3 separate occasions in triplicate. RESULTS: In Caco2 and RIE-1 cells, 10 mM AceK increased carrier-mediated glucose uptake by 20-30% at apical glucose concentrations >25 mM (p 25 mM) glucose concentrations during the 5-min incubation; chelerythrine and cytochalasin B had similar effects. No effect was seen in IEC-6 cells. CONCLUSION: The artificial sweetener AceK, a known sweet taste receptor agonist, has no effect on glucose uptake in low ( 25 mM) in our cell culture models when GLUT2 translocation occurs. The role of artificial sweeteners on glucose uptake appears to act in part by effects on the enterocyte itself. (Support: NIH DK39337-MGS)